Rice Bran Extract Protected against LPS-Induced Neuroinflammation in Mice through Targeting PPAR-γ Nuclear Receptor

PPAR-gamma anti-inflammatory functions have received significant attention since its agonists have been shown to exert a wide range of protective effects in many experimental models of neurologic diseases. Rice bran is very rich in polyunsaturated fatty acids, which are reported to act as PPAR-gamma partial agonists. Herein, the anti-inflammatory effect of rice bran extract (RBE) through PPAR-gamma activation was evaluated in LPS-induced neuroinflammatory mouse model in comparison to pioglitazone (PG) using 80 Swiss albino mice. RBE (100 mg/kg) and PG (30 mg/kg) were given orally for 21 days and LPS (0.25 mg/kg) was injected intraperitoneally for the last 7 days. TNF-alpha and COX-2 brain contents were evaluated by real-time PCR and immunohistochemical analysis. In addition, NF kappa B binding to its response element was evaluated alongside with the effect of treatments on I kappa B gene expression. Furthermore, PPAR-gamma sumoylation was also studied. Finally, histopathological examination was performed for different brain areas. RBE administration was found to protect against the LPS-induced inflammatory effects by decreasing the inflammatory mediator expression in mice brains. It also decreased PPAR-gamma sumoylation without significant effect on I kappa B expression or NF kappa B binding to its response element. The majority of the effects were attenuated in presence of PPAR-gamma antagonist (GW9662). Level of significance was set to P < 0.05. Such findings highlight the agonistic effect of RBE component(s) on PPAR-gamma and support the hypothesis of involvement of PPAR-gamma activation in its neuroprotective effect.

Automated summary

RBE administration was found to protect against the LPS-induced inflammatory effects by decreasing the inflammatory mediator expression in mice brains, potentially through PPAR-gamma activation. Additionally, RBE also decreased PPAR-gamma sumoylation.