Partial protection by 18β Glycrrhetinic acid against Cisplatin induced oxidative intestinal damage in wistar rats: Possible role of NFkB and caspases

Background Cisplatin (CP) is a potent chemotherapeutic agent commonly used for the treatment of various malignancies. It has varied undesirable effects such as nephrotoxicity, intestinal toxicity which limit its wide and extensive clinical usage. 18β-Glycyrrhetinic acid (GA) is a pentacyclic triterpenoid derivative, obtained from the herb liquorice having pharmacological properties such as anti-inflammatory, hepatoprotective and antioxidant. The present study was designed to investigate in vivo efficacy of GA against CP induced small intestinal toxicity. Methods Rats were subjected to prophylactic oral treatment of GA (50 and 100 mg/kg body weight) for 21 days against intestinal toxicity induced by single intra peritoneal injection of CP (10 mg/kg body weight) on day 18th and sacrificed on 21st day. Results The plausible mechanism of CP induced small intestinal toxicity is via deficit in anti-oxidant armory, induction of oxidative stress; TNF-α, NFkB, activation of apoptotic pathway proteins by up regulation of caspases. However prophylactic treatment of GA diminished oxidative stress markers, TNF-α, NFkB expression and enhanced anti-oxidant status, down regulated apoptosis, recovered histopatholgical alterations in small intestine. Conclusion Therefore, results of the present finding provide strong evidence that GA may be a useful modulator in alleviating CP induced intestinal toxicity.