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Mimosa pudica leaf aqueous extract attenuates experimental ulcerative colitis

in rats via suppression of MPO and IL-1β signaling pathways and
improvement of the oxidative status

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DOI: 10.1016/j.phyplu.2024.100559

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Contents lists available at ScienceDirect

Phytomedicine Plus
journal homepage: www.sciencedirect.com/journal/phytomedicine-plus

Mimosa pudica leaf aqueous extract attenuates experimental ulcerative

colitis in rats via suppression of MPO and IL-1β signaling pathways and
improvement of the oxidative status
Henry Awazi Munasi a, Agathe Lambou Fotio a, Michel Archange Fokam Tagne b, Paul
Aimé Noubissi a, *, Mireille Sylviane Dongmo Nguepi c, Nadège Kouémou Emégam a,
Suzy Telma Ntongue Mbemap a, Joseph Mukam Ngakou d, Germain Taiwe Sotoing a,
René Kamgang d, e
a
Department of Animal Biology and Conservation, Faculty of Science, University of Buea, P.O. Box 63, Buea, Cameroon
b
Department of Biological Science, Faculty of Science, University of Ngaoundéré, P.O. Box 454, Ngaoundéré, Cameroon
c
Department of Biochemistry and Molecular Biology, Faculty of Science, University of Buea, P.O. Box 63, Buea, Cameroon
d
Animal Physiology Laboratory, Department of Biology and Animal Physiology, Faculty of Science, University of Yaoundé I, P.O. Box 812, Yaoundé, Cameroon
e
Laboratory of Human Metabolism and Non-Communicable Diseases, Institute of Medical Research and Medicinal Plants Studies (IMPM), Yaoundé, Cameroon

A R T I C L E I N F O A B S T R A C T

Keywords: Background: Colitis for so many years had been considered a disease exclusive only to developed countries;
Acetic acid surprisingly, its incidence is now increasing worldwide. This study investigated Mimosa pudica leaf water extract
Colon inflammation anti-colitis potential on acetic acid-induced colitis in rats.
Body weight
Methods: Following 24 h fasting, 36 rats (both sexes) intrarectally received acetic acid (4%, 1 mL) to induce
Diarrheal feces
Mimosa pudica
colitis. Afterward, they were separated into groups and treated twice a day (for 9 days) with distilled water;
Mimosa pudica (25, 50, or 100 mg/kg); and Prednisolone (5 mg/kg). Body weight and quantity of feces were
recorded. On day 9, animals were sacrificed, colon ulcerations number and weight/length ratio; GSH and MDA
levels; MPO activity, and IL-1β were determined.
Results: Colitis caused a significant drop in animals’ body weight - 30% decrease in colitis control against + 27%
increase in the neutral control rats. Mimosa pudica at 25 mg/kg on day 9 brought a + 7% increase. Colitis led to
an increase in the weight of feces in colitis rats with 14.28 ± 0.98 g (day 8). On this same day, the extract
reduced feces weight (4.42 ± 0.31 g at 100 mg/kg), the number of colon ulcerations, and the mean colon
weight/length ratio (P < 0.001). Colitis conditions increased MDA and decreased GSH. Mimosa pudica reversed
these biomarkers. Colitis caused a marked increase in MPO activity and IL-1β concentration in colitis rats. This
was reversed by the extract.
Conclusions: Overall, our results proved the beneficial effects of Mimosa pudica leaf extract in protecting animals
against colitis.

1. Introduction inflammation of the digestive tract resulting from an inadequate im­

mune response to the gut microbiome (Fokam Tagne et al., 2021a). In
Inflammatory bowel disease (IBD) represents a chronic immune- IBD, inflammation of the intestine mucosa is accompanied by abdominal
mediated inflammatory condition primarily affecting the digestive pain, bloody diarrhea stools, weight loss, and infiltration of macro­
tract (Chen et al., 2019). IBD is marked by the repetitive occurrence of phages and neutrophils producing free radicals, proteolytic enzymes,

List of abbreviations: CD, Crohn’s Disease; GSH, Reduced Glutathione; IBD, Inflammatory Bowel Disease; IL-1β, Interleukine-1 beta; IL-6, Interleukine-6; IL-8,
interleukine-8; MDA, Malondialdehyde; MPO, Myeloperoxidase; SEM, Standard Error of the Means; TNF-α, Tumor Necrosis Factor-alpha; UB-IACUC, University of
Buea Institutional Animal Care and Use Committee; UC, Ulcerative Colitis.
* Corresponding author.
E-mail address: noubiaime@yahoo.fr (P.A. Noubissi).

https://doi.org/10.1016/j.phyplu.2024.100559

Available online 30 March 2024

2667-0313/© 2024 The Author(s). Published by Elsevier B.V. This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-
nc-nd/4.0/).
H.A. Munasi et al.
and cytokines that result in ulceration (Guan, 2019). IBD includes two
idiopathic intestinal diseases which can be differentiated depending on
their location or their depth of involvement in the intestinal wall (Fokam
Tagne et al., 2021b). These are Crohn’s disease (CD) and ulcerative
colitis (UC) (Fakhoury et al., 2014).
UC is a pathology whose etiology is not well known, characterized by
episodes of inflammation of the colon and rectum mucosa and submu­
cosa, resulting in ulcers (Kaur and Goggolidou, 2020). CD represents a
transmural ulceration of any segment of the digestive tract. Most often,
it affects the terminal portion of the ileum and/or the colon (Fokam
Tagne et al., 2021b). Recent investigations provided evidence that IBD
pathogenesis depends on the genetic susceptibility of the host, its in­
testinal microbiome, certain environmental factors, and immunological
abnormalities (Guan, 2019). Among these host factors, mucus abnor­
malities have increasingly gained attention as UC main causative
co-agents. Furthermore, dysbiosis, an altered mucus layer with altered
mucus–microbiota interactions has been associated with IBD (Leoncini
et al., 2024). For decades, IBD has been considered a problem in Western
societies, with the Western lifestyle largely contributing to its patho­
genesis. The incidence of the disease is now rising in developing coun­
tries and is increasingly considered an emerging global disease (Noubissi
et al., 2022). Despite limited epidemiological data from developing
nations, it is now clear that both the incidence and prevalence of IBD are
increasing worldwide. In industrial and urbanized societies, younger
people are more affected (M’Koma, 2013). No sex predominance exists
in ulcerative colitis (Ungaro et al., 2017). The average age of disease
onset is between ages 30 and 40 years (Ungaro et al., 2017). IBD cases
have been recorded in countries in which it had rarely been previously
reported, including South Korea, China, India, Iran, Lebanon, Thailand,
and North Africa (Cosnes et al., 2011). Certain ethnic groups seem to be
more susceptible to UC, but factors such as diet, oral contraceptives,
vaccination, antibiotics, and infections also play a key role (Kaur and
Goggolidou, 2020).
Ulcerative colitis pathophysiology has demonstrated the role of
proinflammatory cytokines such as TNF-α, IL-1β, IL-6, and IL-8, which
are responsible for the production of ROS (Oz et al., 2005; Hyam et al.,
2013). In IBD, the imbalance between ROS and antioxidant activity in­
duces oxidative stress and excessive ROS, and decreases the antioxidant
activity (Hyam et al., 2013). A Decrease in antioxidant biomarkers
following oxidative stress increases IBD incidence (Hyam et al., 2013).
In other words, in UC, the activation of arachidonic acid mediators is
followed by increased production of proinflammatory cytokines such as
IL-6 and TNF-α which, in turn, trigger an increase in MPO, MDA, and
iNOS production (Bejeshk et al., 2023). For the treatment of IBD, ami­
nosalicylates such as sulfasalazine have been among the drugs of choice.
They are used in mild to moderate cases of IBD. Corticosteroids like
prednisone, immunosuppressive drugs such as cyclosporins, antibiotics,
and anti-TNF drugs, are also effective in managing severe to moderate
cases of the disease (Bejeshk et al., 2023). Anti-TNF drugs are one of the
newest methods based on inflammatory processes and intestinal im­
mune response. As one of the most effective drugs against IBD, inflix­
imab significantly improves patient conditions. Unfortunately, none of
the IBD drugs has completely cured the disease. Moreover, they are
costly and are associated with many side effects (Noubissi et al., 2022).
Therefore, the search for alternative and/or complementary remedies
from herbal and traditional medicines has been highly recommended.
Many investigations have focused so far on natural extracts from plants
with anti-inflammatory potential, low toxicity, and minimal side effects.
Adequate and appropriate drugs have been developed from medicinal
plants (Noubissi et al., 2022).
Mimosa pudica L. (Mimosaceae) sometimes referred to as “touch me
not”, “live and die”, “shame plant” or “humble plant” is a semi-erect
subshrub found in tropical America, Australia, India, and Africa,
Cameroon as well. The plant is equipped with numerous recurved thorns
and sensitive soft leaflets that fold and droop at night or when touched
and cooled. Due to these unique bending features, Mimosa pudica has
2
Phytomedicine Plus 4 (2024) 100559
earned the status of ‘curiosity plant’. It stands as a promising candidate
for further investigations according to its pharmacological profile
(Ahmad et al., 2012). The plant, having various polyphenolics and
flavonoid derivatives, has been used in folk medicine for its antidiar­
rheal, antihyperglycemic, anticonvulsant and cytotoxic properties
(Vinothapooshan and Sundar, 2010). Mimosa pudica has been explored
for a wide range of pharmacological activities such as antibacterial (Doss
et al., 2011), anti-inflammatory (Nair and Nair, 2017), antifungal
(Ibrahim et al., 2014), wound healing (Kokane et al., 2009) and
anti-ulcer activity (Ahmad et al., 2012; Singh and Kori, 2022).
Recent investigations revealed the presence of secondary active
metabolites such as Mimosine, Crocetin, Thiamin, Norepinephrine,
Turgorin, Orientin, Isorientin, Vitexin, Isovitexin, Jasmonic acid, D-
pinitol, and Quercetin in Mimosa pudica extracts (Islam et al., 2015).
Furthermore, Islam and collaborators in 2015 demonstrated the
anti-inflammatory potential of Mimosa pudica secondary metabolite,
vitexin which inhibits COX-1 and COX-2 enzymes (Islam et al., 2015),
known to be involved in the synthesis of proinflammatory biomarkers.
So far, no investigation has been conducted to evaluate the
anti-inflammatory potential of this plant on acetic acid-induced colon
inflammation model.
Based on the previous observations, this study therefore aimed to
evaluate the anti-colitis activities of Mimosa pudica leaf aqueous extract
on acetic acid-induced colon inflammation in Wistar rats.
2. Materials and methods
2.1. Drugs and chemicals
Prednisolone (5 mg/kg bw), and distilled water, used in this study
were purchased from local pharmacies. MPO and IL-1β ELISA kits were
purchased from Elabscience, Houston. Acetic acid, trichloroacetic acid,
thiobarbituric acid, phosphoric acid, hydrogen peroxide, hydrochloric
acid, potassium dichromate, tris-base, DTNB (Ellman reagent), and
formalin were purchased from Sigma Aldrich.
2.2. Plant collection, identification, and extract preparation
Fresh young leaves of Mimosa pudica were harvested from the vi­
cinity of the campus of Buea University in June 2020, washed properly
with tap water, and shed dried at room temperature for 2 weeks and
ground into fine powder using an electric blender. The powder obtained
was stored in an air-tight plastic container until the experiment to avoid
microbial contamination. The plant name was checked with https:
//wfoplantlist.org/plant-list, and it was further identified by the Na­
tional Herbarium in Yaounde where a voucher specimen was deposited
under the serial number S4102/HNC. To prepare the extract solution,
234 g of dried fine powder of Mimosa piduca leaves were macerated in
2340 mL of distilled water for 48 h. The mixture then, was filtered using
Whatman No.1 filter paper (Whatman®, England). After filtration, the
filtrate was then oven-dried at 45 ◦ C to obtain a dark-brown semi-solid
crude extract (56.4 g). The extract solution was prepared 30 mins to 1 h
before its administration to the rats, at a volume of 10 mL/kg of body
weight respectively at 25, 50, or 100 mg/kg.
2.3. Animals and ethical consideration
This study was performed on Wistar adult rats with an average age of
2 months with weight ranging from 120 to 150 g. They were purchased
from the animal house of the Laboratory of Human Metabolism and
Non-Communicable Diseases of the Institute of Medical Research and
Medicinal Plants Studies (IMPM), Yaoundé, Cameroon. The rats were
housed in wire bottom cages at room temperature with a natural light/
dark cycle, sufficient aeration, and free access to food (standard rat diet)
and water. The rats were all normal without any disease.
The experiment was conducted according to the guidelines of the
H.A. Munasi et al.
Ethics Committee on the use and care of experimental Animals and
approved by the University of Buea institutional animal care and use
committee (UB-IACUC), authorization number; 14/2022. The Animal
Research Reporting of In Vivo Experiments (ARRIVE) guidelines were
also observed.
2.4. Animal grouping and experimental design
2.4.1. Animal grouping
Thirty-six Wistar rats were randomly divided into six groups of six
animals each. The groups were designated as follows:
• The neutral control group (NC; Group I) which received just distilled
water (10 mL/kg bw).
• The negative control group (NEG C; Group II) was treated with the
vehicle (distilled water, 10 mL/kg bw).
• The test groups (TG; Groups III, IV, and V) each received the aqueous
extract of Mimosa pudica respectively at 25, 50, or 100 mg/kg.
• The positive control group (PC; Group VI) was treated with Pred­
nisolone 5 mg/kg.
2.4.2. Experimental design and induction of colitis
Following a 24-hour fasting period with free access to water, colon
inflammation was induced by intra-rectal administration of 1 mL of
acetic acid 4 %, through a catheter (5 cm) according to the method
previously described (Noubissi et al., 2022). Three days later, colitis
induction was evidenced by bloody and liquid stools (Noubissi et al.,
2022). After colitis induction, the rats were orally treated twice a day
with distilled water, 10 mL/kg for group I (neutral control) and group II
(negative control); Mimosa pudica leaf aqueous extract at 25, 50 and 100
mg/kg respectively (for test groups III-V), or the reference drug, Pred­
nisolone at 5 mg/kg, (Group VI) for 9 days. During the treatment period,
parameters such as body weight variation as well as the weight of watery
stool were recorded. On day 9, after 15 h fasting period, the rats were
terminally anesthetized with a sodium pentobarbital solution (1%, 1
mL/100 g) and the blood was collected in dry tubes and centrifuged
(4000 rpm, 15 mins) to obtain serum. The serum was collected for
biochemical analyses. The colon was equally removed morphologically
examined, and cut-opened to count the number of ulcerations; its length
and weight were measured and the weight/length ratio was calculated
(Fokam Tagne et al., 2021a). Also, livers and kidneys were collected. A
portion of each organ was rinsed in 0.9% NaCl from which 0.5 g was
crushed in Tris–HCl buffer (2.5 M) to make homogenates which were
centrifuged (4000 rpm, 25 mins). The supernatants collected were used
in the evaluation of oxidative stress parameters (MDA and GSH) through
a spectrophotometric method.
2.5. Biochemical assays
2.5.1. Measurement of malondialdehyde (MDA) level
Lipid peroxidation in the colon, liver, and kidney was determined by
measuring the level of MDA according to the method described by Fotio
et al., 2009; 2020 (Fotio et al., 2009; 2020). Briefly, 0.5 mL of tri­
chloroacetic acid (20%) and 1 mL of thiobarbituric acid (0.67%) were
added to 1 mL of tissue homogenate supernatant. The mixture was
incubated in a water bath at 90 ◦ C for 1 h. The mixture was then
centrifuged for 10 mins at 3000 rpm. The absorbance of the collected
supernatant was measured at 546 nm using a spectrophotometer
(UNICO© ULTRA VIOLET). The concentration of MDA was quantified by
the extinction coefficient using the formula:
OD = εCl
Where OD is the optical density; ε is the extinction coefficient (ε =
1.56 × 105 M/cm); C is the concentration of MDA and l is the length of
the cuvette. The concentration was expressed as µmol of MDA per gram
of tissue (Noubissi et al., 2022).
3
Phytomedicine Plus 4 (2024) 100559
2.5.2. Measurement of reduced glutathione (GSH) level
GSH in the colon, liver, and kidney was assayed by the method
described by Ellman (1959). Homogenate supernatant (20 µL) was
mixed with 3 mL of Ellman reagent (5 mg of Disthio-bis 2-nitrobenzoic
acid; DTNB) and 250 mL of phosphate buffer (0.1 M pH 6.5). The
mixture was then kept at room temperature for 1 h and the absorbance
was read using a spectrophotometer (UNICO© ULTRA VIOLET) at 412
nm. GSH concentration was determined by the extinction coefficient (Ɛ)
of 13,600 M − 1 cm− 1 and expressed as µmol per gram of tissue. The
tissue level of GSH was determined using the formula:
A = εCl
Where A is the optical absorbance; ε is the extinction coefficient; C is
the concentration in moles/liter (M); l is the path length (Cm) (Noubissi
et al., 2022).
2.5.3. Myeloperoxidase (MPO) activity and interleukine-1 beta (IL-1β)
level
Myeloperoxidase activity and interleukine-1 beta level were evalu­
ated in serum samples through an ELISA kit following the manufac­
turer’s prescriptions.
2.6. Statistical analysis
The statistical package used for the analysis was GraphPad Prism
version 8.4 for Windows (GraphPad Software, LLC) and Microsoft Excel
2019. Data were expressed as mean ± standard error of the means (S.E.
M.) per group. Statistical differences between control and treated groups
were tested by a one-way analysis of variance (ANOVA), followed by
Dunnett’s multiple comparison test. The differences were considered
significant at P < 0.05.
3. Results
3.1. Effects of Mimosa pudica leaf aqueous extract on body weight of
acetic acid-induced colitis rats
Colitis caused a significant variation in the animal weights all over
the experimental period (Fig. 1). On day 9 the mean animal weight gain
in the neutral control group was 27 % compared to their initial weight.
During this same period, animal weight in the negative control group
dropped by 30 % compared to their initial weight. Treatment with
Mimosa pudica leaf extract prevented extensive weight loss on the same
date (day 9). Weight loss was only about 7, 6, and 6%, at 25, 50, and 100
mg/kg respectively (Fig. 1).
3.2. Effects of Mimosa pudica leaf aqueous extract on the weight of feces
in acetic acid-induced colitis rats
Acetic acid administration resulted in an important release of diar­
rheal feces in colitis rats with, on day 8, 14.28 ± 0.98 g of stools
compared to the neutral control group (5.64 ± 0.28 g) (Fig. 2). On the
same day, Mimosa pudica extract significantly (P < 0.001) and dose-
dependently decreased the weight of feces to 6.22 ± 0.38, 4.68 ±
0.24, and 4.42 ± 0.70 g respectively at 25, 50, and 100 mg/kg compared
to the negative control group (14.28 ± 0.98 g) (Fig. 2). Treatment with
the reference drug Prednisolone also significantly (P < 0.001) decreased
the weight of feces to 4.20 ± 0.06 g (Fig. 2).
3.3. Effects of Mimosa pudica leaf aqueous extract on the number of
macroscopic lesions on the colon of acetic acid-induced colitis rats
Acetic acid caused macroscopic damage on the colon of the affected
animals with 19.80 ± 1.93 ulcerations compared to the normal rats
which had no ulcerations. Treatment with the aqueous extract of Mimosa
pudica leaf aqueous extract at 25, 50 and 100 mg/kg brought a
H.A. Munasi et al. Phytomedicine Plus 4 (2024) 100559

Fig. 1. Body weight variation of acetic acid-induced colitis rats treated with distilled water, Mimosa pudica leaf aqueous extract or Prednisolone.
Results are expressed as percentage body weight (%), n = 6. The differences were considered significant at * P < 0.05, ** P < 0.01 and *** P < 0.001 vs NEG C; a P <
0.05 and b P < 0.01 vs initial weight considered as 100%. NEG C: Negative control group; NC: Neutral control group; TG25, TG50, and TG100: Test groups receiving
Mimosa pudica leaf aqueous extract respectively at 25, 50 or 100 mg/kg; PC: Positive control group treated with Prednisolone 5 mg/kg.

Fig. 2. Quantity of feces of acetic acid-induced colitis rats treated with distilled water, Mimosa pudica leaf aqueous extract or Prednisolone.
The differences were considered significant at *** P < 0.001 vs NEG C. NEG C: Negative control group; NC: Neutral control group; TG25, TG50, and TG100: Test
groups receiving Mimosa pudica leaf aqueous extract respectively at 25, 50 or 100 mg/kg; PC: Positive control group treated with Prednisolone 5 mg/kg.

significant decrease (P < 0.001) in the number of ulcerations, with 8.00 control group (0.170 ± 0.006 mg/cm) (Fig. 4). Also, there was a sig­
± 0.55, 4.60 ± 0.40 and 5.20 ± 0.86 respectively compared to 19.80 ± nificant (P < 0.001) decrease in the colon weight/length ratio in the
1.93 in the negative control group (Fig. 3). Treatment with Prednisolone group treated with Prednisolone, 0.100 ± 0.005 mg/cm Fig. 4.
also reduced the number of ulcerations to 6.80 ± 0.49 (Fig. 3).

3.5. Effects of Mimosa pudica leaf aqueous extract on oxidative stress

3.4. Effects of Mimosa pudica leaf aqueous extract on the colon weight/
length ratio in acetic acid-induced colitis rats
Colitis administration brought about an increase in the mean colon
weight/length ratio, 0.170 ± 0.006 mg/cm in the negative control
group against 0.090 ± 0.001 mg/cm (P < 0.001) in the neutral control
group Fig. 4. Treatment with Mimosa pudica leaf aqueous extract
significantly (P < 0.001) and dose-dependently decreased the colon
weight/length ratio: 0.120 ± 0.002, 0.110 ± 0.009, and 0.100 ± 0.005
mg/cm respectively at 25, 50 and 100 mg/kg compared to the negative
biomarkers of acetic acid-induced colitis rats
3.5.1. Effects of Mimosa pudica leaf aqueous extract on MDA
concentration
Colitis was accompanied by a significant (P < 0.001) increase of
MDA in the colon (10.31 ± 0.31 µmol/g), liver (6.17 ± 0.04 µmol/g)
and kidney (5.63 ± 0.51 µmol/g) of non-treated rats compared to the
neutral control group with 4.87 ± 0.10, 1.66 ± 0.12 and 3.13 ± 0.13
µmol/g respectively Fig. 5. Mimosa pudica at 25, 50, and 100 mg/kg,
significantly (P < 0.001) decreased MDA concentration in the colon

4
H.A. Munasi et al. Phytomedicine Plus 4 (2024) 100559

Fig. 3. Number of macroscopic lesions on colon of acetic acid-induced colitis rats treated with distilled water, Mimosa pudica leaf aqueous extract or Prednisolone.
The differences were considered significant at *** P < 0.001 vs NEG C. NEG C: Negative control group; NC: Neutral control group; TG25, TG50, and TG100: Test
groups receiving Mimosa pudica leaf aqueous extract respectively at 25, 50 or 100 mg/kg; PC: Positive control group treated with Prednisolone 5 mg/kg.

Fig. 4. Colon weight/length ratio of acetic acid-induced colitis rats treated with distilled water, Mimosa pudica leaf aqueous extract, or Prednisolone.
The differences were considered significant at *** P < 0.001 vs NEG C. NEG C: Negative control group; NC: Neutral control group; TG25, TG50, and TG100: Test
groups receiving Mimosa pudica leaf aqueous extract respectively at 25, 50 or 100 mg/kg; PC: Positive control group treated with Prednisolone 5

(8.39 ± 0.10, 5.42 ± 0.11, and 5.45 ± 0.16 µmol/g); in the liver (5.34 ±
0.17, 4.45 ± 0.16 and 3.52 ± 0.06 µmol/g); and in the kidney (4.50 ±
0.17, 3.62 ± 0.04 and 3.14 ± 0.05 µmol/g) respectively Fig. 5. Decrease
in MDA concentration in the colon, liver, and kidney was also significant
(P < 0.001) in the Prednisolone-treated group (4.90 ± 0.41, 3.08 ±
0.19, and 3.20 ± 0.03 µmol/g) respectively Fig. 5.
3.5.2. Effects of Mimosa pudica leaf aqueous extract on GSH concentration
Colitis induction brought about a significant decrease of glutathione
concentration in the colon, liver, and kidney of non-treated colitis
control rats with 2.31 ± 0.21, 5.33 ± 0.24, and 5.65 ± 0.17 µmol/g
against 6.47 ± 0.14, 11.74 ± 0.46 and 14.09 ± 0.80 µmol/g
respectively, in the normal rats Fig. 6. Mimosa pudica leaf aqueous
extract respectively at 25, 50, and 100 mg/kg significantly and dose-
dependently increased glutathione concentration in the colon, 2.54 ±
0.13 µmol/g, 4.83 ± 0.07 (P < 0.01) and 6.55 ± 0.15 µmol/g (P <
0.001); in the liver (8.25 ± 0.41, 8.37 ± 0.35, 10.82 ± 0.17 µmol/g, (P
< 0.01, P < 0.001 and P < 0.001); and in the kidney (7.68 ± 0.21, 8.47
± 0.11, 10.16 ± 0.22 µmol/g, (P < 0.05, P < 0.01 and P < 0.001) Fig. 6.
Increase in glutathione levels in the colon, liver, and kidney was also
significant (P < 0.01) in the group treated with Prednisolone with 6.35
± 0.12, 12.31 ± 0.72, and 9.38 ± 0.22 µmol/g respectively Fig. 6.

5
H.A. Munasi et al. Phytomedicine Plus 4 (2024) 100559

Fig. 5. MDA concentration of acetic acid-induced colitis rats treated with distilled water, Mimosa pudica leaf aqueous extract or Prednisolone.
The differences were considered significant at ** P < 0.01 and *** P < 0.001 vs NEG C. NEG C: Negative control group; NC: Neutral control group; TG25, TG50, and
TG100: Test groups receiving Mimosa pudica leaf aqueous extract respectively at 25, 50 or 100 mg/kg; PC: Positive control group treated with Prednisolone 5 mg/kg.

Fig. 6. GSH concentration in acetic acid-induced colitis rats treated with distilled water, Mimosa pudica leaf aqueous extract or Prednisolone.
The differences were considered significant at * P < 0.05, ** P < 0.01 and *** P < 0.001 vs NEG C. NEG C: Negative control group; NC: Neutral control group; TG25,
TG50, and TG100: Test groups receiving Mimosa pudica leaf aqueous extract respectively at 25, 50 or 100 mg/kg; PC: Positive control group treated with Pred­
nisolone 5 mg/kg.

Fig. 7. MPO activities in acetic acid-induced colitis rats treated with distilled water, Mimosa pudica leaf aqueous extract or Prednisolone.
The differences were considered significant at *** P < 0.001 vs NEG C. NEG C: Negative control group; NC: Neutral control group; TG25, TG50, and TG100: Test
groups receiving Mimosa pudica leaf aqueous extract respectively at 25, 50 or 100 mg/kg; PC: Positive control group treated with Prednisolone 5 mg/kg.

6
H.A. Munasi et al.
3.5.3. Effects of Mimosa pudica leaf aqueous extract on MPO levels of
acetic acid-induced colitis rats
Colitis brought about a significant (P < 0.001) increase in the serum
MPO levels of rats in the negative control group with 812.10 ± 3.49 U/L
compared to the neutral control group, 211.50 ± 16.98 U/L Fig. 7.
Treatment with Mimosa pudica leaf aqueous extract at 25, 50 and 100
mg/kg significantly (P < 0.001) decreased the serum MPO levels
respectively, to 137.00 ± 17.70, 233.30 ± 24.27 and 316.70 ± 25.64 U/
L compared to the negative control group with 812.1 ± 3.49 U/L Fig. 7.
Prednisolone also led to a significant (P < 0.001) reduction in the serum
MPO levels with 244 ± 7.87 U/L compared to the negative control group
with 812.1 ± 3.49 U/L Fig. 7.
3.5.4. Effects of Mimosa pudica leaf aqueous extract on IL-1β serum
concentration of acetic acid-induced colitis rats
Acetic acid administration caused a significant (P < 0.001) increase
in the IL-1β concentration in the serum of rats in the negative control
group with 15.25 ± 1.08 pg/mL compared to the neutral control group
with 9.87 ± 0.50 pg/mL Fig. 8. Mimosa pudica extract brought a sig­
nificant (P < 0.001) dose-dependent decrease in the serum IL-1β con­
centration at 25, 50 and 100 mg/kg respectively to 10.57 ± 0.50, 8.34 ±
0.35 and 7.51 ± 0.32 pg/mL compared to the negative control group
(15.25 ± 1.08 pg/mL) Fig. 8. Treatment with the reference drug Pred­
nisolone also brought a significant (P < 0.001) reduction in the serum IL-
1β concentration of rats in the positive control with 6.36 ± 0.14 pg/mL
compared to the negative control group Fig. 8.
4. Discussion
Inflammatory Bowel Disease remains a serious public health problem
worldwide. For its treatment, aminosalicylates such as sulfasalazine
have been among the drugs of choice. Corticosteroids like prednisone,
immunosuppressive drugs such as cyclosporins, antibiotics, and anti-
TNF drugs, are also effective in managing severe to moderate cases of
the disease (Bejeshk et al., 2023). Anti-TNF drugs are one of the newest
methods based on inflammatory processes and intestinal immune
response. However, none of these drugs has completely cured the dis­
ease. Moreover, they are costly and are associated with many side effects
(Noubissi et al., 2022). Therefore, the search for alternative and/or
complementary remedies from herbal and traditional medicines has
been highly recommended. In the current study, we investigated the
effects of the aqueous extract of Mimosa pudica leaves on acetic
acid-induced colon inflammation, precisely on the related parameters
such as body weight, colon weight/length ratio, oxidative stress
Fig. 8. IL-1β concentrations in acetic acid-induced colitis rats treated with distilled water, Mimosa pudica leaf aqueous extract or Prednisolone.
The differences were considered significant at *** P < 0.001 vs NEG C. NEG C: Negative control group; NC: Neutral control group; TG25, TG50, and TG100: Test
groups receiving Mimosa pudica leaf aqueous extract respectively at 25, 50 or 100 mg/kg; PC: Positive control group treated with Prednisolone 5 mg/kg.
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Phytomedicine Plus 4 (2024) 100559
biomarkers, MPO, and IL-1β a proinflammatory cytokine.
Many investigations revealed the presence of secondary active me­
tabolites such as Mimosine, Crocetin, Thiamin, Norepinephrine, Tur­
gorin, Orientin, Isorientin, Vitexin, Isovitexin, Jasmonic acid, D-pinitol,
and Quercetin in Mimosa pudica extracts (Islam et al., 2015). These
secondary metabolites were shown to exhibit anti-inflammatory po­
tential, with vitexin inhibiting COX-1 and COX-2 enzymes (Islam et al.,
2015), known to be involved in the synthesis of proinflammatory
biomarkers.
The experimental induction of ulcerative colitis by intrarectal
administration of a low concentration of acetic acid (usually 3–5 %) is a
well-known model for the study of inflammatory bowel disease (Aleisa
et al., 2014). The underlying mechanisms involving acetic acid-induced
local inflammation, desquamation, and loss of mucosal integrity leading
to epithelial injury are due to acetic acid conversion to a protonated
form that diffuses into the epithelium and subsequently dissociates to
form protons (Kandhare et al., 2012). This subsequently can result in the
acidification of the cellular structure and the induction of inflammatory
bowel disease (Kumar et al., 2014). Chemotaxis and inflammatory cell
infiltration and the release of mediators and proteases occur, eventually
resulting in ulceration, hemorrhage, necrosis, and intestinal tissue
damage (Rafeeq et al., 2021). Also, the influx of inflammatory cells such
as neutrophils into the injured colon ruptures the colonic barrier, and
releases inflammatory mediators (such as cytokines and arachidonic
acid metabolites) and ROS, resulting in oxidative damage (Ali et al.,
2017).
In the current study, intra-rectal administration of acetic acid caused
inflammation and diarrhea followed by a significant weight loss in all
the rats of the negative control group and test groups compared to those
in the neutral group which experienced a steady increase in their body
weight. Weight loss in IBD could be attributed to a certain number of
different processes. Among others, a deficiency of nutrients resulting
from reduced appetite, food aversion or malabsorption, and rapid loss of
body fluid through colorectal bleeding and diarrhea (Owusu et al.,
2020). IBD in its nature, is inflammatory, and it results in a generalised
catabolic state. It has been demonstrated an increased resting energy
expenditure and proinflammatory cytokines release (with anorexic ef­
fect) during acute flares in CD. The inflammatory state observed in this
disease has been related to altered levels of some metabolic hormones
including adiponectin, leptin, and ghrelin which are known to influence
satiety. Also, IBD pathophysiological processes are associated with the
malabsorption of both micronutrients and macronutrients (Elsherif
et al., 2014). Furthermore, IBD is characterized by increased gastrocolic
reflex and a variety of symptoms such as pain, which are often associated
H.A. Munasi et al.
with food avoidance (Elsherif et al., 2014).
The reduction in body weight as it was observed in the current
investigation may also have been due to excess dehydration and nutrient
malabsorption caused by the disruption of the epithelial cell layers of the
intestine by the acetic acid. Also, both TNF-α and IL-6 contribute to body
weight loss in colitis by promoting the release of neuropeptides that
suppress appetite and precipitate cachexia (Owusu et al., 2020). Treat­
ment with the different doses of the aqueous extract of Mimosa pudica
prevented the drastic loss in body weight observed in the colitis rats.
This extract may contain secondary active metabolites which could
stimulate appetite or reduce nutrients and body fluid loss by preserving
the intestine integrity.
Macroscopic examination of the colon revealed an increased number
of colon ulcerations, as well as the colon weight/length ratio. An in­
crease in cell infiltration and edema often corresponds to an increase in
colon weight/length ratio (Adakudugu et al., 2020). Macroscopic
changes of the colonic mucosa in ulcerative colitis can be attributed to
extreme edema, necrosis, hyperplasia of goblet cells, and inflammatory
cell infiltration (Yu and Liu, 2021). Treatment with Mimosa pudica
significantly reduced the colon weight/length ratio. This may have been
due to a reduction in extreme edema and inflammatory cell infiltration
by the plant.
Oxidative stress is a pathological condition that results from an
imbalance between the amount of ROS produced in tissues and cells, and
the ability of a biological system to detoxify these products (Pizzino
et al., 2017). Oxidative stress is known to play a key role in the initiation
and progression of IBD. Substantial evidence suggests that IBD is asso­
ciated with an imbalance between antioxidant potential and ROS pro­
duction, which creates oxidative stress as a result of either an increased
production of ROS or a decrease in antioxidant activity (Balmus et al.,
2016). The different ROSs include superoxide (O−2 ), nitric oxide (NO),
hydroxyl radical (OH− ), hydroperoxyl radical (O2H), hydrogen peroxide
(H2O2), and singlet oxygen (O2) (Balmus et al., 2016). Experimentally
induced colitis in animals is characterized by oxidative damage and an
imbalance between antioxidant and oxidant substances (Al-rejaie et al.,
2013). The acetic acid-induced colon inflammation model has been
known to cause vascular dilatation and accumulation of white blood
cells, as well as an increase in blood flow which causes increased pro­
duction of oxygen, generation of excessive free radicals, and ROS
(Al-rejaie et al., 2013). ROS are mainly produced by mitochondria,
during both physiological and pathological conditions. O•− 2 can be
formed by cellular respiration, by lipoxygenases (LOX) and cyclo­
oxygenases (COX) during the arachidonic acid metabolism, and by
endothelial and inflammatory cells (Al-Gubory et al., 2012). They
perform important functions as second messengers in different intra­
cellular signaling pathways keeping the cell in homeostasis with its
surroundings. They provoke indiscriminate destruction of cellular mol­
ecules, leading therefore to loss of function or cell death (Tejchman
et al., 2021). Cells make use of an important antioxidant defensive
system mainly based on enzymatic components like SOD, CAT, and
glutathione peroxidase (GPx), to protect themselves from ROS-induced
cellular damage (Deponte, 2013).
MDA levels in this study were higher in the non-treated colitis rats
compared to the neutral control and treated groups. MDA is a by-product
of lipid peroxidation occurring in the tissue. In ulcerative colitis, levels
of MDA in the plasma increase significantly, and this is used as an
important diagnosis of patients with inflammatory bowel disease (Ali
et al., 2017). Lipid peroxidation develops progressively in cellular and
subcellular membranes during oxidative stress, causing irreversible
damage to cellular function (Govindarasu et al., 2021). Acetic acid may
have exacerbated the effect of lipid peroxidation due to the acidification
of the epithelium and tissue injury thereby increasing MDA levels. There
was a significant reduction in MDA levels as a result of Mimosa pudica
treatment which suggests that it is capable of reversing the oxidative
stress in acetic acid-induced colitis rats by inhibiting lipid peroxidation
in cells of the colonic mucosa.
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Phytomedicine Plus 4 (2024) 100559
GSH is a primary antioxidant agent crucial in tissue repair as it
prevents free radicals from damaging the mucosa, which is also essential
for wound healing (Ahmed et al., 2022). Its reduced form, GSH, a more
prevalent agent, is a soluble antioxidant that is highly expressed in the
cytoplasm, nucleus, and mitochondria. GSH, together with three related
enzymes, glutathione peroxidase (GPX), glutathione reductase (GSR),
and glutathione S-transferases (GST), forms an antioxidant barrier in the
gut mucosa (Tian et al., 2017). The GSH cycle is an important intra­
cellular anti-oxidant defense system (Cagin et al., 2016). It is used as a
substrate for the activity of several anti-oxidant enzymes particularly
GPX which is a glutathione-dependent enzyme. In the presence of GSH,
GPX detoxifies H2O2 into H2O and O2 molecules. GSH subsequently loses
a hydrogen atom and oxidized glutathione (GSSG) is formed (El-Beltagi
and Mohamed, 2013). Glutathione reductase leads to the formation of
GSH from GSSG (Cagin et al., 2016). During colon inflammation, GSH
level decreases resulting in severe injury to the colon mucosa (Olami­
losoye et al., 2018). The current results show that acetic acid adminis­
tration resulted in the reduction of colonic tissue GSH concentration.
Mimosa pudica leaf aqueous extract significantly increased the GSH
concentration in the colon of the treated animals. This increase in GSH
levels showed that the extract might have reduced the level of reactive
oxygen species and prevented the inhibition of the antioxidant enzymes
or triggered their synthesis which in turn ameliorated the oxidative
damage caused by acetic acid in the colitis rats.
MPO is a peroxidase enzyme found primarily in neutrophils’ azur­
ophilic granules (Olamilosoye et al., 2018) and much lower concentra­
tions in monocytes and macrophages (Shivanandappa et al., 2011). The
level of MPO activity is directly proportional to the neutrophil concen­
tration in the inflamed tissue (Shivanandappa et al., 2011) and elevated
levels of MPO indicate neutrophil infiltration and inflammatory cascade
dysfunction which have been documented not only in animal models but
also in patients with IBD (Rafeeq et al., 2021). In the current study, an
increase of MPO activity in colonic tissue indicates inflammation dam­
age resulting from neutrophil infiltration into the colon of colitis rats.
Treatment with Mimosa pudica aqueous extract at various doses signif­
icantly reduced the serum MPO activity in the treated groups. This
reduction might have been due to secondary active metabolites found in
Mimosa pudica like alkaloids, mucilage, tannins, non-protein amino acid
(mimosine), flavonoid C-glycosides, sterols, terpenoids, and fatty acids
(Johnson et al., 2014), which are known to inhibit vascular perme­
ability, inflammatory cell infiltration, and edema (Soliman et al., 2016).
Proinflammatory cytokines play a very important function in IBD
pathogenesis. They influence the mucosal immune system, modify the
integrity of epithelium, and organize the invasion and release of neu­
trophils and macrophages, resulting in colonic injury (Yu and Liu,
2021). Due to the migration of granulocytes and other leukocytes to the
inflamed mucosa and superficial ulcers, the result is the overproduction
of pro-inflammatory cytokines, which indicate the severity of the disease
(Fatani et al., 2016). Cytokines including TNF-α, IL-1β and IL-6 are
considered pro-inflammatory because once produced by activated
macrophages, they stimulate the liberation of other cytokines, arach­
idonic acid metabolites, and lytic enzymes by intestinal macrophages,
neutrophils, smooth muscle cells, fibroblasts and epithelial cells, pro­
moting edema, fibrosis and necrosis (Fakhfouri et al., 2010). IL-1β can
induce an elevated neutrophil count and promote the migration of
neutrophils (Dinarello, 2009), T cell activation and survival (Ben-sasson
et al., 2009). In our study IL-1β was elevated in the serum of animals in
the negative control group, indicating severe inflammation. Treatment
with the Mimosa pudica leaf aqueous extract provided a significant
dose-dependent reduction in serum IL-1β levels. This shows that the
extract might have reduced the production of neutrophils by preventing
the recruitment of macrophages and leukocytes with a consequent
reduction in secretion of proinflammatory cytokines thereby reducing
inflammation.
H.A. Munasi et al.
5. Conclusion
This work focused on the study of anti-colitis effects of the leaf
aqueous extract of Mimosa pudica on acetic acid-induced colon inflam­
mation in Wistar rats. The extract inhibited weight loss and decreased
diarrheal feces emission and the colon weight/length ratio in acetic acid
colitis rats. The extract also increased anti-oxidant biomarkers in the
colon, liver, and kidney tissues. Furthermore, it reduced colitis rats’
myeloperoxidase activity and IL-1β serum level. This, however, dem­
onstrates the anti-colitis benefits of the plant which, therefore, stands as
a potential candidate for the development of an alternative treatment
against ulcerative colitis.
CRediT authorship contribution statement
Henry Awazi Munasi: Conceptualization, Data curation, Formal
analysis, Funding acquisition, Investigation, Methodology, Resources,
Writing – original draft. Agathe Lambou Fotio: Conceptualization,
Methodology. Michel Archange Fokam Tagne: Data curation, Writing
– review & editing. Paul Aimé Noubissi: Writing – review & editing,
Visualization, Validation, Supervision, Software, Resources, Project
administration, Methodology, Investigation, Funding acquisition,
Formal analysis, Data curation, Conceptualization. Mireille Sylviane
Dongmo Nguepi: Data curation, Formal analysis, Writing – review &
editing. Nadège Kouémou Emégam: Data curation, Formal analysis,
Methodology. Suzy Telma Ntongue Mbemap: Investigation, Writing –
original draft. Joseph Mukam Ngakou: Data curation, Investigation,
Methodology, Software. Germain Taiwe Sotoing: Writing – review &
editing, Resources, Validation, Visualization. René Kamgang: Writing –
review & editing, Validation, Supervision, Project administration.
Declaration of competing interest
The authors declare that they have no known competing financial
interests or personal relationships that could have appeared to influence
the work reported in this paper.
Acknowledgment
The authors sincerely acknowledge the Institute of Medical Research
and Medicinal Plants Studies (IMPM), Yaoundé, Cameroon, for
providing laboratory facilities during this study.
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