Naringin is neuroprotective in
ischemia and other disease models. However, the effects of
naringin are unknown after
traumatic brain injury (TBI). The present study explored the role of
naringin for neuroprotection in TBI rats. TBI was performed with the weight drop technique, and
naringin was given orally at a dose of 100 mg/kg/day. The neurological scores, tissue
edema, and oxidative stress/
inflammation parameters [
malondialdehyde (MDA),
superoxide dismutase,
nitric oxide,
inducible nitric oxide synthase (iNOS), as well as interleukin-1β (IL-1β)] were measured. Compared to
sham controls, TBI rats displayed obvious sensorimotor dysfunction, significant
brain edema, and elevated oxidative and inflammatory molecules. Although a 7-day pre-treatment of
naringin was unable to reverse these pathological changes, a 14-day continual treatment (7 days before and 7 days after the TBI) attenuated the increases in MDA and
nitric oxide; enhanced the activation of
superoxide dismutase; depressed the over-activation of iNOS; down-regulated the over-expression of IL-1β; and reduced the cortex
edema. Additionally, the TBI-induced behavioral dysfunction was reduced. These results suggest that
naringin treatment can attenuate cellular and histopathological alterations and improve the sensorimotor dysfunction of TBI rats, which may be partly due to the attenuation of oxidative and inflammatory damages.