CYP2E1 inhibition and NF_κB Signaling Pathway are Involved in the Protective Molecular Effect of against Acetaminophen-induced acute Hepatotoxicity in Rats.

The present study aimed to estimate the potential and the molecular mechanism of the hydro-ethanolic extract of against acetaminophen (AC) induced hepatotoxicity. Four groups of female Wistar rats (n=6) was formed to study the hepatoprotective effect of extract against acetaminophen overdose (2 g/kg): Groups N and AC received orally tap water for 03 days and Groups + AC and N+: received orally extract (400 mg/kg). After 1hour (h) of the last dose administered, the paracetamol solution (2 g/kg) is administered orally for group AC and + AC. The hydroethanolic extract of shows strong antioxidant activity "". After 24 h, a single dose of acetaminophen increased significantly serum aspartate aminotransferase (AST), alanine aminotransferase (ALT) and the activity of alkaline phosphatase (ALP) significantly and decreased total protein and albumin levels compared to the normal group. These alterations are confirmed by histological observations with inflammation markers (congestion, inflammatory cells infiltration). These observed effects are mainly due to the over-expression of the and genes marked in this study by quantitative RT-PCR. Also, acetaminophen overdose leads to activation of the mitochondrial permeability transition (MPT). leading to hepatocyte necrosis. Pretreatment with before acetaminophen administration removes all previously observed biochemical, histological. and mitochondrial manifestations. These results suggest that has a potent antioxidant power and an interesting hepatoprotective activity against acetaminophen toxicity partly due to the inhibition of and genes expression.