Antioxidative Biomolecular protective activity of Napoleonaea vogelii Against Cyclophosphamide-induced hepatotoxicity in Rats

Abstract

Cyclophosphamide (CYP) is an anticancer drug that undergoes extensive metabolic biotransformation into pro-oxidant metabolites that are implicated in severe undesirable side effects in multiple organs. Napoleonaea vogelii (NV), is a tropical flowering plant with phytochemicals that have been shown to possess medicinal properties utilized in the management of cancer, dermatosis and peptic ulcer. There is paucity of information on its potential against toxicological profile of alkylating cytotoxic agents such as cyclophosphamide. This study therefore investigated the mitigative influence of NV against CYP-induced liver injury in rat. The rats intraperitoneally received cyclophosphamide (2 mg/kg) or orally co-treated with Napoleonaea vogelii (400 mg/ kg) daily for 14 days. Co-treatment with Napoleonaea vogelii buffered the alteration on hematological parameters caused by cyclophosphamide. Napoleonaea vogelii in treatment group also mitigated impaired liver function by significant reduction in the activities of transaminases and the alkaline phosphatase relative to cyclophosphamideintoxicated rats. CYP also altered redox status through significant reduction in serum total thiol, hepatic activities of catalase, superoxide dismutase and reduced glutathione concentration with concomitant elevation in serum advanced oxidized protein products-AOPPs and hepatic malondialdehyde concentration relative to control. However, co-treatment with Napoleonaea vogelii reestablished the serum and hepatic antioxidant status. Moreover, the increase in serum levels of proinflammatory markers: TNF-alpha, NF-KB and MPO were observed in treated rats exposed to benzene as compared to control. Meanwhile, co-treatment with Napoleonaea vogelii profers abrogative influence on the surge elevation observed in TNF-alpha, NF-KB and MPO in treated rats when compared to the CYP-exposed rats. Overall, Napoleonaea vogelii protected against oxidative hepatic injury and hematological derangement caused by cyclophosphamide in rats.