Curcumin Phytosome Modulates Aluminum-induced Hepatotoxicity Via Regulation of Antioxidant, Bcl-2, and Caspase-3 in Rats

Increasing entrance of aluminum chloride (AlCl) in many fields exposes human beings to its biotoxicity. Thereby, the present study assesses the potential ameliorative role of curcumin phytosome (CP) on AlCl-induced hepatotoxicity. Rats were divided into four groups (n = 6): group 1 served as control; group 2 received CP (200 mg CP/kg b.wt) for 21 days; group 3 injected three doses of AlCl (30 mg/kg/body weight) every 5 days intraperitoneally; group 4 received CP for 7 days prior to AlCl and then received CP concurrently with AlCl for another 14 days. AlCl markedly increased (P < 0.05) the concentrations of AST, ALT, ALP, LDH, total bilirubin, and LPO as well as depleted (P < 0.05) albumin, GSH, SOD, and GPx stores in comparison to the control group. These biochemical alterations supported by the lesion observed in histological sections, increasing the expression of caspase-3 and decreasing the expression of Bcl-2. Treatment with CP modulates the hepatic dysfunction, boosting the endogenous antioxidant status, downregulating the expression of caspase-3, and upregulating the expression of Bcl-2. This hepatic ameliorative effect may be mediated by the ability of CP to repair the oxidant/antioxidant equilibrium rather than its ability to suppress apoptosis.