PHYTOTHERAPY RESEARCH

Phytother. Res. 26: 34–38 (2012)

Published online 28 April 2011 in Wiley Online Library
(wileyonlinelibrary.com) DOI: 10.1002/ptr.3515

The Mechanism of Sesame Oil in Ameliorating

Experimental Autoimmune Encephalomyelitis in
C57BL/6 Mice

A. Ghazavi1 and G. Mosayebi2*

1
Infectious Disease Research Center, Department of Immunology and Microbiology, School of Medicine, Arak University of Medical
Sciences, Arak, Iran
2
Molecular and Medicine Research Center, Department of Immunology and Microbiology, School of Medicine, Arak University of
Medical Sciences, Arak, Iran

Experimental autoimmune encephalomyelitis (EAE) is a Th1 cell‐mediated autoimmune disease of the CNS
that serves as an animal model for multiple sclerosis (MS). The study investigated the effectiveness of treatment
with sesame oil on the development of EAE. EAE was induced in 8 week old C57BL/6 mice with an emulsion of
MOG35‐55. Therapy with sesame oil (4 mL/kg/day as oral gavage) was started on day 3 before the
immunization. IFN‐gamma and IL‐10 production from cultured spleen supernatants were determined by the
ELISA method. The results showed that daily oral gavage of sesame oil significantly reduced the clinical
symptoms of EAE in C57BL/6 mice. In addition, sesame oil‐treated mice displayed a significantly delayed
disease onset. Mononuclear cells isolated from spleen of sesame oil‐treated mice showed a significant decrease in
the production of IFN‐gamma compared with control mice (p = 0.001). IL‐10 production was also enhanced in
splenic mononuclear cells in sesame oil‐treated mice. The ratio of IFN‐gamma to IL‐10 in sesame oil‐treated
EAE mice was significantly less than in non‐treated EAE mice (p = 0.01). This report indicates that sesame oil
therapy protected mice from developing EAE by reducing IFN‐gamma secretion. Thus, sesame oil treatment
may be effective in MS patients by immunomodulating the Th1 immune response. Copyright © 2011 John Wiley
& Sons, Ltd.
Keywords: multiple sclerosis; experimental autoimmune encephalomyelitis; sesame oil; cytokines.

INTRODUCTION number of lipid‐soluble antioxidants have been isolated

Experimental autoimmune encephalomyelitis (EAE) is
an inflammatory demyelinating disease of the central
nervous system (CNS) that has similar aspects to
multiple sclerosis (MS) (Basso et al., 2008). MS is an
immunological disease mediated by CD4 + T cells
(Pender and Greer, 2007). CD4+T cells can develop
into Th1 and Th2 subsets characterized by different
cytokine production. Th1 cells produce inflammatory
cytokines, such as interferon (IFN)‐gamma and enhance
cellular immunity. Th2 cells produce different types of
interleukins (IL‐4, 5, 6 and 10), and induce humoral
immunity (Mosmann et al., 1986; Rao and Avni, 2000).
IFN‐gamma produced by Th1 cells activates macro-
phages and microglia, which are considered as main
effectors of demyelination and axonal damage (Huitinga
et al., 1990; Renno et al., 1998; Trapp et al., 1998). However,
suppression of the Th1 immune response or promotion
of the Th2 immune response is effective in the treatment
of MS disease (Adorini, 2004).
Sesame seeds (Sesamum indicum, Linn., Pedaliaceae)
have long been categorized as a traditional health food in
Iran and other Asian countries. They have also been
used traditionally to treat inflammatory disorders. A
* Correspondence to: Ghasem Mosayebi, Molecular and Medicine
Research Center, Department of Immunology and Microbiology, School
of Medicine, Arak University of Medical Sciences, Arak, Iran 3848176941.
E‐mail: gmosayebi@yahoo.com
from sesame seeds, including sesaminol, sesamolin, P1
and pinoresinol; sesame oil has been found to contain
considerable amounts (up to 1.5%) of the sesame lignans,
sesamin and sesamolin (Jan et al., 2009; Kang et al., 1998).
The lignans present in sesame oil are thought to be
responsible for its antioxidant and antiinflammatory
properties (Sankar et al., 2005; Utsunomiya et al., 2000).
In a previous study it was shown that intraperitoneal
injection of sesame oil reduced the clinical symptoms of
EAE and increased the total antioxidant capacity in serum
of C57BL/6 mice with EAE (Mosayebi et al., 2007).
Some reports refer to the allergic reactions caused by
sesame oil (Gangur et al., 2005; Kanny et al., 1996; Oiso
et al., 2008). Since the Th2 cells interfere with allergic
reactions by producing IL‐4, there is the probability that
sesame oil, by supporting the Th2 immune response, will be
able to inhibit Th1 immune responses. However, no
previous study has examined the use of sesame oil in the
treatment of MS or other Th1 cell‐mediated inflammatory
diseases of the CNS. The present study examined the effect
of sesame oil on the day of onset and severity of EAE
and the Th cytokine profile in C57BL/6 mice with EAE.
MATERIALS AND METHODS
Mice. Male C57BL/6 mice were obtained from the Pasteur
Institute of Iran, at an appropriate age (6–8 weeks). The
mice (weighing about 20 ± 2 g) were divided randomly

Received 24 January 2011

Copyright © 2011 John Wiley & Sons, Ltd. Accepted 22 March 2011
 SESAME OIL AND EXPERIMENTAL AUTOIMMUNE ENCEPHALOMYELITIS
into two groups, each with 10 mice. The mice were housed
in the animal house at Immunologic Research Center of
Arak University of Medical Sciences in accordance with
all Institutional Ethical and Health guidelines.
Sesame oil treatment. All mice were fed for the duration
of the experiment with tap water and mouse fodder. In
the experimental group (n = 10), mice were given sesame
oil (4 mL/kg/day, orally). Sesame oil obtained from
Iranian white sesame seeds contains saturated fat 14%,
monounsaturated fat 40%, polyunsaturated fat 42%,
cholesterol 0%, carbohydrate 0%, protein 0%, sodium
0% and potassium 0%. One mL sesame oil consists of
5.84 mg sesamol (Sadeghi et al., 2009). Control mice
(n = 10) were given phosphate‐buffered saline (PBS),
(4 mL/kg/day, orally). Sesame oil and PBS injection were
started on day 3 before the immunization and continued
to day 25 post immunization.
Induction of experimental autoimmune encephalomyelitis
(EAE). Mice were inoculated s.c. in the flank with 0.1 mL
of an emulsion containing 200 µg of the encephalitogenic
peptide MOG35‐55 (MEVGWYRSPFSRVVHLYRNGK;
Diapharm Ltd, Russia) and an equal volume of complete
Freund’s adjuvant (Sigma, St Louis, MO) supplemented
with 4 mg/mL Mycobacterium tuberculosis H37RA (Difco,
Detroit, MI, USA). Mice were injected intraperitoneally
with 400 ng of pertussis toxin (Sigma) on the day of
immunization and 2 days later (Costa et al., 2003).
Clinical evaluation of EAE. Following the encephalito-
genic challenge, the mice were monitored daily and
neurological impairment was scored on an arbitrary
clinical score as follows: 0, no clinical sign; 1, partial loss
of tail tonicity; 2, complete loss of tail tonicity; 3, flaccid
tail and abnormal gait; 4, hind leg paralysis; 5, hind leg
paralysis with hind body paresis; 6, hind and foreleg
paralysis; 7, moribund or death. The relapse was defined
when a mouse developed an increase of the clinical score
(more than 1) accompanied by weight loss. Under
recommendation of the animal ethics committee, the
mice were killed on 25 day post immunization (Mosayebi
et al., 2007).
Spleen cells preparation. On day 25 post‐immunization,
the mice were killed by CO2 inhalation, and the spleens
were removed. Spleens were washed in RPMI (modifi-
cation with 5 mM HEPES, 100 U/mL of penicillin and
100 µg/mL of streptomycin, all from Gibco, Life Tech-
nologies, Inc., Gaithersburg, MD). The spleens were
punctured repeatedly with a pair of forceps to release the
spleen cells. Low density mononuclear cells were
collected after standard separation on Ficoll‐Paque
(Pharmacia Biotech, Uppsala, Sweden), and washed in
RPMI with 10% heat‐inactivated fetal bovine serum
(FBS). The number of viable cells was assessed by trypan
blue exclusion. The cells were then resuspended in RPMI
supplemented with 10% FBS, and used for the prolifera-
tion assay and cytokine detection.
Proliferation of splenocytes. Proliferation was checked
by the MTT assay method (Bounous et al., 1992). A total
of 3 × 103 cells in 200 μL RPMI 1640 supplemented with
10% FBS were stimulated with 20 µg/mL MOG35‐55
peptide or 5 µg/mL ConA. The plates were then placed in
a 5% CO2, 37 °C incubator for 72 h. Twenty microliters of
Copyright © 2011 John Wiley & Sons, Ltd.
35
5 mg/mL MTT(3‐(4,5dimethyldiazol‐2‐yl)‐2,5‐dipenyl;
Sigma‐Aldrich, St Louis, MO) was added to the cells,
followed by incubation for 4 h. After centrifugation, the
medium was removed, and 200 μL of DMSO was added
to each well. Then, the optical density at 540 nm was
measured by microtiter plate reader (Stat Fax2100,
USA). The experiments were performed in triplicate
sets. Blastogenic responses for the MTT assay were
expressed as the mean stimulation index (SI) by dividing
the OD values of stimulated cells (C) minus relative cell
numbers of unstimulated cells (C) by the relative OD
values of unstimulated cells. SI = (C − C)/CMTT.
Cytokines assay. Splenocytes isolated from mice on day
25 post‐immunization at a density of 2 × 106 cells/mL
were incubated in 1 mL cultures in the presence or
absence MOG35–55 peptide (20 µg/mL) and placed in a
5% CO2, 37 °C incubator for 96 h. To quantitative IFN‐
gamma and IL‐10 production, supernatants were
collected and the amounts of IFN‐gamma and IL‐10
in the supernatants were quantified by ELISA kit
(R&D Systems) according to the manufacturer’s proto-
col. Ninety‐six‐well plates were coated with rat anti‐
mouse IFN‐gamma and IL‐10 antibody in coating buffer
(pH 9.6) and incubated overnight. After blocking,
samples and standards at 1:2 serial dilutions of IFN‐
gamma and IL‐10 (standard curve) were added to the
plates and incubated for 60 min at room temperature.
After that, biotinylated rat anti‐mouse IFN‐gamma and
IL‐10 mAbs were added and incubated for another
60 min. HRP‐conjugated streptavidin were then added
for 30 min. After further washings, TMB substrate was
added to incubate for 30 min, followed by addition of
0.18 mM H2SO4 solution to stop the reaction and reading
at 450 nm was obtained.
Statistical analysis. Statistical analysis was performed
with the Mann‐Whitney U‐test to compare the mean
maximal score, mean onset day and levels of cytokines.
Values of p < 0.05 were considered significant.
RESULTS
Clinical score
The current study investigated the effect of sesame oil
administration on evaluation of EAE (Fig. 1). All animals
in the sesame oil‐treated and control groups developed
clinical signs of EAE. The onset of the first clinical scores
occurred on days 10 and 14 post‐immunization in control
group and sesame oil‐treated EAE, respectively
(p = 0.02). The mean maximum clinical scores of the
sesame oil‐treated group were significantly lower than
that in the control group (6 ± 0.7 and 4.8 ± 0.5, respectively,
p = 0.01).
Proliferation assay
The study examined the mechanism underlying the
amelioration of disease by sesame oil‐treated EAE
mice. To examine whether cell proliferation against
MOG35‐55 peptide is influenced by sesame oil treatment,
mononuclear cells obtained from the spleen of either
Phytother. Res. 26: 34–38 (2012)
36 A. GHAZAVI AND G. MOSAYEBI
Figure 1. Mean clinical course of MOG35‐55‐induced EAE in C57BL/6 mice. Values are means and standard deviations for the 10 mice tested
daily in each group.
sesame oil‐treated or control mice (10 mice in each group)
were stimulated with 20 µg/mL of MOG35‐55 peptide or
5 µg/mL ConA. The results show that no significant
differences were demonstrated in the cell proliferations
between the control and sesame oil‐treated groups (Fig. 2).
Cytokine assay
The effects of sesame oil on immunomodulation of the
immunological response were examined by detection
IL‐10 and IFN‐gamma. There was a significant differ-
ence between the level of IFN‐gamma production in the
culture supernatants of cells from control or sesame oil‐
treated mice (p = 0.001) (Table 1). The concentration of
IL‐10 in supernatants of cells from sesame oil‐treated
mice (69 ± 48) was higher than in the control group
Figure 2. Effects of sesame oil on the proliferation of spleen cells
of EAE mice. 25 days after EAE induction, the mononuclear cells
obtained from spleen of sesame oil‐treated and non‐treated EAE
mice were stimulated with 20 µg/mL MOG35‐55 peptide or 5
µg/mL ConA for 72 h. Increase in cell number was measured by the
MTT assay method. Each value represents the mean ± SE (n = 10).
Copyright © 2011 John Wiley & Sons, Ltd.
(58 ± 24) but this difference was not significant. The
ratio of IFN‐gamma to IL‐10 in the sesame oil‐treated
EAE mice (7.6) was significantly less than in the non‐
treated EAE mice (16.89) (p = 0.001).
DISCUSSION
In this study, a protective effect of sesame oil on EAE
induced in C57BL/6 mice was demonstrated. Sesame oil
significantly delayed the disease onset of EAE and
reduced the maximum clinical scores. The mechanism by
which sesame oil exhibits its observed beneficial effect is
still unknown, but some studies showed that sesame oil
has potent antiinflammatory and antioxidant effects
(Akimoto et al., 1993; Chavali et al., 2001; Hsu et al.,
2005). In addition, sesame oil consumption influences
beneficially the blood glucose, lipid peroxidation and
antioxidant levels in streptozotocin diabetic rats
(Ramesh et al., 2005).
Assessment of the cytokine pattern in response to
MOG3‐55 re‐stimulation indicated that sesame oil
treatment led to a reduction IFN‐gamma secretion as
demonstrated for splenocyte cultures. Although im-
mune cells from sesame oil‐treated EAE mice did not
show a diminished proliferative response toward
MOG35‐55, the levels of IFN‐gamma in the supernatants
of splenocytes were lower on sesame oil treatment
compared with the control mice, but the levels of IL‐10 in
sesame oil‐treated mice were not significantly higher
than those in the non‐treated EAE mice. IFN‐gamma is a
pro‐inflammatory cytokine that plays an important role
in inflammatory and autoimmune diseases, such as MS
(Mana et al., 2006; Popko et al., 1997). The frequencies of
IFN‐gamma secreting myelin antigen‐reactive T cells are
increased in blood and especially in the cerebrospinal
fluid of MS patients, compared with the controls
(Soderstrom et al., 1993; Sun et al., 1991). Administration
of IFN‐gamma to MS patients exacerbates the disease
(Panitch et al., 1985). In addition, lymphocytes from MS
Phytother. Res. 26: 34–38 (2012)
 SESAME OIL AND EXPERIMENTAL AUTOIMMUNE ENCEPHALOMYELITIS
Table 1. IFN‐gamma and IL‐10 production by MNCs obtain from spleen of sesame oil‐treated and non‐treated EAE mice
Group IFN‐gamma (ρg/mL)
No
+MOG35‐55
MOG‐EAE + PBS 10 980 ± 42
MOG‐EAE + sesame oil 10 527 ± 40
p value 0.001
Data given represent mean ± standard deviation.
N.S, not significant.
patients produce elevated levels of IFN‐gamma in vitro
compared with the controls (Hirsch et al., 1985). The
protective effect of IFN‐beta therapy in MS patients has
been attributed to down‐regulation of IFN‐gamma
production (Furlan et al., 2000).
There are considerable data demonstrating that
under particular conditions and/or in specific tissues
IFN‐gamma act to down‐regulate inflammation. Admin-
istration of anti‐IFN‐gamma antibody to mice or rats
aggravated EAE (Espejo et al., 2001). On a susceptible
background, IFN‐gamma‐/‐ mice developed more severe
EAE, whereas IFN‐gamma‐/‐ mice on resistant genetic
backgrounds become sensitive to EAE (Chu et al., 2000).
Animals lacking the gene for IFN‐gamma are much more
EAE susceptible (Ferber et al., 1996; Krakowski and
Owens, 1996). However, the molecular mechanisms that
would explain why in certain situations the antiinflam-
matory properties of IFN‐gamma remain largely elusive.
In addition, histological examination of brain tissues
demonstrated reduced levels of infiltration of leuko-
cytes in the sesame oil‐treated EAE mice (Mosayebi
et al., 2007). Sesame oil has an antiinflammatory effect
and it has been suggested that sesame oil or constituents
of sesame oil induce growth arrest and apoptosis of
cancer. Recently, it was reported that sesame oil, a
vegetable oil enriched with n‐6 polyunsaturated fatty
acids attenuated the growth and metastasis of EL4
lymphoma (Salem, 2005). The mechanism of the sesame
oil effect on reducing IFN‐γ production and disease
intensity is not clear. Some performed studies show that
sesame oil causes apoptosis induction in cancer cells.
REFERENCES
Adorini L. 2004. Immunotherapeutic approaches in multiple
sclerosis. J Neurol Sci 223: 13–24.
Akimoto K, Kitagawa Y, Akamatsu T et al. 1993. Protective effects
of sesamin against liver damage caused by alcohol or carbon
tetrachloride in rodents. Ann Nutr Metab 37: 218–224.
Basso AS, Frenkel D, Quintana FJ et al. 2008. Reversal of axonal
loss and disability in a mouse model of progressive multiple
sclerosis. J Clin Invest 118: 1532–1543.
Bounous DI, Campagnoli RP, Brown J. 1992. Comparison of MTT
colorimetric assay and tritiated thymidine uptake for lympho-
cyte proliferation assays using chicken splenocytes. Avian Dis
36: 1022–1027.
Chavali SR, Utsunomiya T, Forse RA. 2001. Increased survival
after cecal ligation and puncture in mice consuming diets
enriched with sesame seed oil. Crit Care Med 29: 140–143.
Chu CQ, Wittmer S, Dalton DK. 2000. Failure to suppress the
expansion of the activated CD4 T cell population in
interferon gamma‐deficient mice leads to exacerbation of
experimental autoimmune encephalomyelitis. J Exp Med
192: 123–128.
Costa O, Divoux D, Ischenko A, Tron F, Fontaine M. 2003.
Optimization of an animal model of experimental autoimmune
encephalomyelitis achieved with a multiple MOG(35‐55)
peptide in C57BL6/J strain of mice. J Autoimmun 20: 51–61.
Copyright © 2011 John Wiley & Sons, Ltd.
37
IL‐10 (ρg/mL)
−MOG35‐55 +MOG35‐55 −MOG35‐55
5 ± 3.7 58 ± 24 26 ± 20
13 ± 12 69 ± 48 24 ± 10
N.S N.S N.S
Salem and colleagues showed that prescribing sesame
oil prevents the growth and metastasis of enteric EL4
lymphoma in C57BL/6 mice (Salem, 2005). Further-
more, Miyahara and colleagues, by effecting sesamolin
on Molt‐4 B range lymphoid cells, showed that
sesamolin from sesame seeds induces apoptosis in these
cells (Miyahara et al., 2001). So sesame oil may cause a
decline in IFN‐γ production and EAE intensity by
apoptosis induction or inhibition of inflammatory cell
proliferation.
CONCLUSION
Our study shows, for the first time, that sesame oil
reduces the severity of disease and proliferation of
leukocytes in EAE mice. The findings suggest that
sesame oil might be potentially useful for the treatment
of MS.
Acknowledgement
This work was supported by Research Council of Arak University of
Medical Sciences.
Conf lict of Interest
The authors declare that there is no conflict of interest.
Espejo C, Penkowa M, Saez‐Torres I et al. 2001. Treatment with
anti‐interferon‐gamma monoclonal antibodies modifies experi-
mental autoimmune encephalomyelitis in interferon‐gamma
receptor knockout mice. Exp Neurol 172: 460–468.
Ferber IA, Brocke S, Taylor‐Edwards C et al. 1996. Mice with a
disrupted IFN‐gamma gene are susceptible to the induction of
experimental autoimmune encephalomyelitis (EAE). J Immunol
156: 5–7.
Furlan R, Bergami A, Lang R et al. 2000. Interferon‐beta treatment
in multiple sclerosis patients decreases the number of circulating
T cells producing interferon‐gamma and interleukin‐4. J Neu-
roimmunol 111: 86–92.
Gangur V, Kelly C, Navuluri L. 2005. Sesame allergy: a growing food
allergy of global proportions? Ann Allergy Asthma Immunol 95:
4–11; quiz 11–13, 44.
Hirsch RL, Panitch HS, Johnson KP. 1985. Lymphocytes from
multiple sclerosis patients produce elevated levels of gamma
interferon in vitro. J Clin Immunol 5: 386–389.
Hsu DZ, Su SB, Chien SP et al. 2005. Effect of sesame oil on
oxidative‐stress‐associated renal injury in endotoxemic rats:
involvement of nitric oxide and proinflammatory cytokines.
Shock 24: 276–280.
Huitinga I, van Rooijen N, de Groot CJ, Uitdehaag BM, Dijkstra CD.
1990. Suppression of experimental allergic encephalomyelitis
Phytother. Res. 26: 34–38 (2012)
38 A. GHAZAVI AND G. MOSAYEBI
in Lewis rats after elimination of macrophages. J Exp Med
172: 1025–1033.
Jan KC, Ho CT, Hwang LS. 2009. Elimination and metabolism of
sesamol, a bioactive compound in sesame oil, in rats. Mol Nutr
Food Res 53 (Suppl 1): S36–S43.
Kang MH, Naito M, Tsujihara N, Osawa T. 1998. Sesamolin
inhibits lipid peroxidation in rat liver and kidney. J Nutr 128:
1018–1022.
Kanny G, De Hauteclocque C, Moneret‐Vautrin DA. 1996. Sesame
seed and sesame seed oil contain masked allergens of
growing importance. Allergy 51: 952–957.
Krakowski M, Owens T. 1996. Interferon‐gamma confers resist-
ance to experimental allergic encephalomyelitis. Eur J Im-
munol 26: 1641–1646.
Mana P, Linares D, Fordham S, Staykova M, Willenborg D. 2006.
Deleterious role of IFNgamma in a toxic model of central
nervous system demyelination. Am J Pathol 168: 1464–1473.
Miyahara Y, Hibasami H, Katsuzaki H, Imai K, Komiya T. 2001.
Sesamolin from sesame seed inhibits proliferation by inducing
apoptosis in human lymphoid leukemia Molt 4B cells. Int J Mol
Med 7: 369–371.
Mosayebi G, Ghazavi A, Salehi H, Payani MA, Khazae MR. 2007.
Effect of sesame oil on the inhibition of experimental
autoimmune encephalomyelitis in C57BL/6 mice. Pak J Biol
Sci 10: 1790–1796.
Mosmann TR, Cherwinski H, Bond MW, Giedlin MA, Coffman RL.
1986. Two types of murine helper T cell clone. I. Definition
according to profiles of lymphokine activities and secreted
proteins. J Immunol 136: 2348–2357.
Oiso N, Yamadori Y, Higashimori N, Kawara S, Kawada A. 2008.
Allergic contact dermatitis caused by sesame oil in a topical
Chinese medicine, shi‐un‐ko. Contact Dermat 58: 109.
Panitch HS, Francis GS, Hooper CJ, Merigan TC, Johnson KP.
1985. Serial immunological studies in multiple sclerosis
patients treated systemically with human alpha interferon.
Ann Neurol 18: 434–438.
Pender MP, Greer JM. 2007. Immunology of multiple sclerosis.
Curr Allergy Asthma Rep 7: 285–292.
Copyright © 2011 John Wiley & Sons, Ltd.
Popko B, Corbin JG, Baerwald KD, Dupree J, Garcia AM. 1997.
The effects of interferon‐gamma on the central nervous
system. Mol Neurobiol 14: 19–35.
Ramesh B, Saravanan R, Pugalendi KV. 2005. Influence of sesame
oil on blood glucose, lipid peroxidation, and antioxidant status
in streptozotocin diabetic rats. J Med Food 8: 377–381.
Rao A, Avni O. 2000. Molecular aspects of T‐cell differentiation.
Br Med Bull 56: 969–984.
Renno T, Taupin V, Bourbonniere L et al. 1998. Interferon‐gamma in
progression to chronic demyelination and neurological deficit
following acute EAE. Mol Cell Neurosci 12: 376–389.
Sadeghi N, Oveisi MR, Mannan Hajimahmoodi M, Behrooz Jannat B,
Mazaheri M, Sadollah Mansouri S. 2009. The contents of
sesamol in Iranian sesame seeds. Iran J Pharm Res 8: 101–105.
Salem ML. 2005. Systemic treatment with n‐6 polyunsaturated
fatty acids attenuates EL4 thymoma growth and metastasis
through enhancing specific and non‐specific anti‐tumor
cytolytic activities and production of TH1 cytokines. Int
Immunopharmacol 5: 947–960.
Sankar D, Sambandam G, Ramakrishna Rao M, Pugalendi KV.
2005. Modulation of blood pressure, lipid profiles and redox
status in hypertensive patients taking different edible oils. Clin
Chim Acta 355: 97–104.
Soderstrom M, Link H, Sun JB et al. 1993. T cells recognizing
multiple peptides of myelin basic protein are found in blood
and enriched in cerebrospinal fluid in optic neuritis and
multiple sclerosis. Scand J Immunol 37: 355–368.
Sun JB, Olsson T, Wang WZ et al. 1991. Autoreactive T and B cells
responding to myelin proteolipid protein in multiple sclerosis
and controls. Eur J Immunol 21: 1461–1468.
Trapp BD, Peterson J, Ransohoff RM, Rudick R, Mork S, Bo L.
1998. Axonal transection in the lesions of multiple sclerosis.
N Engl J Med 338: 278–285.
Utsunomiya T, Chavali SR, Zhong WW, Forse RA. 2000. Effects of
sesamin‐supplemented dietary fat emulsions on the ex vivo
production of lipopolysaccharide‐induced prostanoids and
tumor necrosis factor alpha in rats. Am J Clin Nutr 72:
804–808.
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