Zea mays, Stigma maydis prevents and extenuates acetaminophen-perturbed oxidative onslaughts in rat hepatocytes.

Pharm Biol

a Phytomedicine and Phytopharmacology Research Group, Department of Plant Sciences , University of the Free State-QwaQwa Campus, Phuthaditjhaba , South Africa.

Published: November 2016

Context: Zea mays L. (Poaceae) Stigma maydis is an underutilized product of corn cultivation finding therapeutic applications in oxidative stress-related disorders.

Objectives: This study investigated its aqueous extract against acetaminophen (APAP)-perturbed oxidative insults in rat hepatocytes.

Materials And Methods: Hepatotoxic rats were orally pre- and post-treated with the extract (at 200 and 400 mg/kg body weight) and vitamin C (200 mg/kg body weight), respectively, for 14 days. Liver function, antioxidative and histological analyses were thereafter evaluated.

Results: The APAP-induced marked (p < 0.05) increases in the activities of alkaline phosphatase, alanine aminotransferase, aspartate aminotransferase, gamma glutamyl transferase and the concentrations of bilirubin, oxidized glutathione, protein carbonyls, malondialdehyde, conjugated dienes, lipid hydroperoxides and fragmented DNA were dose-dependently extenuated in the extract-treated animals. The extract also significantly (p < 0.05) improved the reduced activities of superoxide dismutase, catalase, glutathione reductase and glutathione peroxidase as well as total protein, albumin and glutathione concentrations in the hepatotoxic rats. These improvements may be attributed to the bioactive constituents as revealed by the gas chromatography-mass spectrometric chromatogram of the extract. The observed effects compared favourably with vitamin C and are informative of hepatoprotective and antioxidative attributes of the extract and were further supported by the histological analysis.

Conclusion: The data from the present findings suggest that Stigma maydis aqueous extract is capable of preventing and ameliorating APAP-mediated oxidative hepatic damage via enhancement of antioxidant defence systems.

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http://dx.doi.org/10.1080/13880209.2016.1178307DOI Listing

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