Abstract:
The aim of this study was determined the effects
of Hesperidin (HP) on neuronal damage in brain tissue
caused by Experimental allergic encephalomyelitis
(EAE), an established model of multiple sclerosis in
C57BL/J6 mice. To explore 40 mice were equally divided
into four groups: (1) Control, (2) EAE, (3) HP, and (4)
HP ? EAE. 14 days after induction of EAE with MOG35-
55 and pertussis toxin, the mice treated with HP at the
doses of 50 mg/kg/day for 7 days subcutaneously. To our
results HP treatment prevents the oxidative stress caused
by EAE via a decrease in lipid peroxidations and increase
in elements of the antioxidant defense systems in brain
tissue. Also, EAE elevate the IL-17, express the pro-in-
flammatory cytokines, and caspase-3-like immunreactivity,
show apoptosis, staining in EAE mice brain and increased
the incidence of histopathological damage. However, immonohistochemical
and histological changes were reversed
with HP. Moreover, elevated TNF-a and IL-1b levels, a
result of EAE, were decreased in serum and neurological
deficits as clinical signs were reversed with HP treatment in
EAE mice, given HP. In conclusion, HP treatment
effectively prevents oxidative, immunological and histological
damage in the brain caused by EAE. It was thought
that the beneficial effects of HP are likely a result of its
strong antioxidant and anti-inflammatory properties.
