Continual naringin treatment benefits the recovery of traumatic brain injury in rats through reducing oxidative and inflammatory alterations.

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.