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Background  This study aims to assess the hepatoprotective potential of  Commelina nudiflora  against CCl 4 -induced hepatic injury in rats.    Method  Antioxidant activities were determined. Phytochemical analysis was performed by gas chromatography mass spectrometry (GCMS). In the in vivo study, Sprague Dawley rats were pretreated with  C. nudiflora  (150, 300, and 450 mg kg body weight (b.wt.)) once daily for 14 days followed by two doses of CCl 4  (1 ml/kg b.wt.). After 2 weeks, the rats were sacrificed and hepatoprotective analysis was performed.    Results  In vitro studies have shown that the extract possessed strong antioxidant activity and has ability to scavenge 2,2-diphenyl-2-picrylhydrazyl-free radicals effectively. GCMS analysis of the  C. nudiflora  extract revealed the presence of various bioactive compounds. Administration of  C. nudiflora  significantly reduced the impact of CCl 4  toxicity on serum markers of liver damage, serum aspartate transaminase (AST), and alanine transaminase (ALT).  C. nudiflora  also increased antioxidant levels of hepatic glutathione (GSH) and antioxidant enzymes and ameliorated the elevated hepatic formation of malondialdehyde (MDA) induced by CCl 4  in rats. Histopathological examination indicated that  C. nudiflora  protect the liver from the toxic effect of CCl 4  and healed lesions such as necrosis, fatty degeneration, and hepatocyte injury as irregular lamellar organization and dilations in the endoplasmic reticulum. The immunohistochemical studies revealed that pretreatment of  C. nudiflora  decreased the formation of 4-hydroxy-2-nonenal (HNE)-modified protein adducts and 8-hydroxy-2′-deoxyguanosine (8-OHdG). Furthermore, overexpression of the proinflammatory cytokines TNF-α, IL-6, and prostaglandin E2 is also reduced.    Conclusion  These findings exhibited the potential prospect of  C. nudiflora  as functional ingredients to prevent ROS-related liver damage.

environmental health and preventive medicine

The potential protective effect of Commelina nudiflora L. against carbon tetrachloride (CCl4)-induced hepatotoxicity in rats, mediated by suppression of oxidative stress and inflammation