Tribulus terrestris ameliorates carbon tetrachloride-induced hepatotoxicity in male rats through suppression of oxidative stress and inflammation

Kilany, Omnia E.; El-Beltagy, Marwa A.; El-Sherbeeny, Nagla A.

Tribulus terrestris ameliorates carbon tetrachloride-induced hepatotoxicity in male rats through suppression of oxidative stress and inflammation

2020

Kilany, Omnia E. | El-Beltagy, Marwa A. | El-Sherbeeny, Nagla A.

Hepatoprotection is a goal for the harmful effect of several hepatotoxic agents. The present study has been executed to assess the useful impacts of Tribulus terrestris (TT) and silymarin (SLM) against carbon tetrachloride (CCL₄)-induced hepatotoxicity. Forty-two male rats were partitioned into six groups: group I: received 0.3% CMC-Na in distilled water, group II: TT (500 mg/kg BW, orally), group III: SLM (200 mg/kg, orally) for 14 consecutive days (on days 11 and 12 intraperitoneal corn oil), group IV: CCL₄, group V: TT (500 mg/kg BW) plus CCL₄, and group VI: SLM (200 mg/kg orally) plus CCL₄. The CCL₄ was administered (2.0 ml/kg BW) intraperitoneal on days 11 and 12. Sera were collected for assessment of hepatic injury markers and pro-inflammatory cytokines. Additionally, liver tissue oxidative stress, lipid peroxidation, histopathological examination, and immunohistochemical analysis (Bax and bcl-2) were done. CCL₄ injection induced significant reductions in hepatic antioxidants while increased hepatic lipid peroxidation as well as serum hepatic injury biomarkers and pro-inflammatory cytokines. The histopathological examination showed necrotic and degenerative changes in the hepatic tissue, while immunohistochemical analysis revealed marked hepatic expression of activated Bax, and bcl-2, following CCL₄ injection. TT pretreatment significantly improved all examined parameters and restored the hepatic architecture. The current study illustrated that TT effectively alleviates hepatic oxidative damage, apoptosis, and inflammation, induced by acute CCL₄ intoxication. In this manner, TT has promising cytoprotective powers against hepatotoxicity induced by CCL₄.

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