Amelioration of Nephrotoxicity in Mice Induced by Antituberculosis Drugs Using Ensete ventricosum (Welw.) Cheesman Corm Extract

BACKGROUND: Antituberculosis drugs are antimicrobial agents important for treating a communicable disease called tuberculosis. Despite their importance, antituberculosis drugs such as isoniazid and rifampicin have severe adverse effects like nephrotoxicity with acute renal failures. Ensete ventricosum (Welw.) Cheesman is a nutritional herbaceous perennial plant, and it has indigenous ethnomedicinal values for the society. This study aimed to evaluate the protective role of the Ensete ventricosum (Welw.) Cheesman corm extract (EVCE) against nephrotoxicity induced by isoniazid and rifampicin in mice. METHODS: The present study was conducted on thirty Swiss albino mice randomly allocated into five groups. Group-I (only distilled water), Group-II (only isoniazid 75 mg/kg and rifampicin150 mg/kg), Group-III (isoniazid and rifampicin along with 200 mg/kg EVCE), Group-IV (isoniazid and rifampicin along with 400 mg/kg EVCE), and Group-V (isoniazid and rifampicin along with silymarin) were treated for thirty days. At the end of the study, the experimental animals were sacrificed after being injected with anesthetic drug, blood was drawn for a kidney function test, and the kidney was also taken from each experimental animal for histopathological evaluation. Data were entered and analyzed by using one-way ANOVA of SPSS version 25. Results and Conclusion. Serum levels of creatinine, blood urea nitrogen (BUN), and uric acid of the Group-II mice were significantly (P < 0.01) elevated, and serum levels of total proteins and albumin of Group-II mice were significantly (P < 0.01) decreased as compared to Group-I. The group of mice treated with an EVCE reinstated those derangements. The kidney section of Group-II mice showed an abnormality in kidney structure; however, these deformities were not detectable in group-IV mice. The EVCE has sufficient nephroprotective potential against antituberculosis drug-induced kidney injury.