Coleus vettiveroides ethanolic root extract protects against thioacetamide‐induced acute liver injury in rats

Abstract

Acute liver injury is caused by various factors, including oxidative stress and inflammation. Coleus vettiveroides, an ayurvedic medicinal plant, is known to possess antioxidant, antibacterial, and antidiabetic properties. In this current study, we investigated the protective effect of C. vettiveroides ethanolic root extract (CVERE) against thioacetamide (TAA)‐induced acute liver injury in rats. A single dose of TAA (300 mg/kg, b.w., i.p.) was administered to induce acute liver injury. The treatment groups of rats were concurrently treated with CVERE (125 and 250 mg/kg, b.w., p.o.) and silymarin (100 mg/kg, b.w., p.o.), respectively. After 24 h of the experimental period, TAA‐induced liver injury was confirmed by increased activity of serum transaminases and malondialdehyde levels in liver tissue, decreased levels of antioxidants, upregulated expression of the inflammatory marker gene, and altered liver morphology. Whereas CVERE simultaneous treatment inhibited hepatic injury and prevented the elevation of serum aspartate and alanine transaminases, alkaline phosphatase, and lactate dehydrogenase activities. CVERE attenuated TAA‐induced oxidative stress by suppressing lipid peroxidation and restoring antioxidants such as superoxide dismutase, catalase, and reduced glutathione. Further, CVERE treatment was found to inhibit nuclear factor κB‐mediated inflammatory signaling, as indicated by downregulated pro‐inflammatory cytokines including tumor necrosis factor‐α and interleukin‐1β. Our findings suggest that CVERE prevents TAA‐induced acute liver injury by targeting oxidative stress and inflammation.

Thymoquinone protects thioacetamide‐induced chronic liver injury by inhibiting TGF‐β1/Smad3 axis in rats

“…TAA has been known to induce oxidative stress‐mediated chronic liver injury. [ 11 ] In an in vitro model, TAA treatment induced lipid peroxidation via ROS production in hepatocytes isolated from rat liver. [ 40 ] In vivo experimental studies have also confirmed that TAA administration can induce lipid peroxidation and downregulation of enzymic and non‐enzymic antioxidants in the liver tissue of experimental animals.…”

“…A single dose of TAA has been shown to induce centrilobular necrosis in the liver via oxidative stress and inflammation in rats. [ 10,11 ] Besides, intermittent administration of TAA has also been shown to induce chronic liver injury via oxidative stress and inflammation‐mediated activation of transforming growth factor‐β (TGF‐β) signalling pathways. [ 12,13 ] Therefore, in this study, we have used TAA to induce chronic liver injury in rats.…”