Evening Primrose Oil Enriched with Gamma Linolenic Acid and D/L-Alpha Tocopherol Acetate Attenuated Carbon Tetrachloride-Induced Hepatic Injury Model in Male Rats via TNF-α, IL1 β and IL6 pathway.

Abstract

The modulatory role of primrose oil (PO) supplementation enriched with γ-linolenic acid and D/L-alpha tocopherol acetate against a carbon tetrachloride (CCl4)-induced liver damage model was assessed in this study. Twenty male albino rats were divided into four groups. The control group received corn oil orally. The PO group received 10 mg/kg P O orally. The CCl4 group received 2 mL/kg CCl4 orally and PO/CCl4 group; received PO and 2 mL/kg CCl4 orally. The relative liver weight was recorded. Serum liver enzymes, hepatic malondialdehyde (MDA), hepatic reduced glutathione (GSH) and the expression of hepatic tumor necrosis factor-alpha (TNF-α), interleukin 1 beta (IL1β), and interleukin 6 (IL6) were assessed. The binding affinities of γ-linolenic acid and D/L-alpha tocopherol constituents with IL1β, IL6 and TNF-α were investigated using molecular docking simulations. Histopathological and electron microscopic examinations of the liver were performed. The results indicated that CCl4 elevated serum liver enzyme and hepatic MDA levels, whereas GSH levels were diminished. The upregulation of IL1β, IL6, and TNF-α gene expressions were induced by CCl4 treatment. PO/CCl4 treated group showed amelioration of hepatic injury biomarkers and oxidative stress. Restoration of histopathological and ultrastructural alterations while downregulation the gene expressions of TNF-α, IL1 β and IL6 were observed. In conclusion, evening primrose oil enriched with γ-linolenic acid and D/L-alpha tocopherol acetate elicited a potential amelioration of CCl4-induced hepatic toxicity.