Pomegranate action in curbing the incidence of liver injury triggered by Diethylnitrosamine by declining oxidative stress via Nrf2 and NFκB regulation.

Unearthing and employment of healthy substitutes is now in demand to tackle a number of diseases due to the excessive repercussions of synthetic drugs. In this frame of reference pomegranate juice (PGJ) is a boon comprising of anthocyanins and hydrolysable tannins, known for its anti-oxidant and anti-inflammatory properties. Despite various documented roles of PGJ, there are no studies on antifibrotic potential in NDEA-induced mammalian liver fibrotic model. Hepatic fibrosis in rats was induced by the intra-peritoneal injection of NDEA (10 mlkg-1b.wt. of 1% NDEA) in two weeks. Biochemical, histopathological and ultra-structural studies were carried out on control, fibrotic and treated rats. The liver function indices and LPO were increased significantly by intoxication of NDEA. The antioxidant status was disturbed with the decrease in SOD, GST and catalase in the liver and membrane-ATPases as well. Histopathological observations by H&E, M&T, picro-sirius and ultra-structural scrutiny by SEM and TEM indicated liver damage and increase in COX2 and α-SMA by NDEA which was successfully rectified by the supplementation of PGJ. PGJ abrogates liver fibrosis instigated by NDEA in Wistar rats by declining oxidative stress via regulation of Nrf2 and NFκB. These findings point towards pomegranate as a potential and efficacious therapeutic agent against liver fibrosis.