Coleus vettiveroides ethanolic root extract protects against thioacetamide-induced acute liver injury in rats.
Kadmad Abdul Hameed Mohamed AzarEzhilarasan DevarajKarthik Shree HariniMunusamy KarthickMani UthirappanPublished in: Cell biochemistry and function (2023)
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.
Keyphrases
- liver injury
- drug induced
- oxidative stress
- nuclear factor
- dna damage
- ischemia reperfusion injury
- toll like receptor
- hydrogen peroxide
- poor prognosis
- rheumatoid arthritis
- gene expression
- dna methylation
- intensive care unit
- hepatitis b virus
- newly diagnosed
- transcription factor
- mass spectrometry
- long non coding rna
- immune response
- mouse model
- signaling pathway
- respiratory failure
- single molecule
- high speed