Abstract
Context: Hepatotoxicity is a therapeutic predicament that affects the clinical use of cisplatin (CPT). Ipomoea aquatica is traditionally used for the treatment of some diseases. This study examined the protective effect of the ethanolic leaf extract of Ipomoea aquatica (EEIA) against CPT-induced hepatotoxicity in albino rats.
Materials and Methods: Fifty-four adult male albino rats randomized into nine groups (six rats in each group) were treated orally with EEIA (100, 200, and 400 mg/kg) daily for 7 days and CPT (6 mg/kg) intraperitoneally on day 5 and 7, respectively. On day 8, the rats were anesthetized; blood samples were collected and evaluated for plasma liver function markers. Liver samples were harvested and evaluated for biochemical parameters and histology.
Statistical Analysis: Data are presented as mean ± standard error of the mean (SEM). Statistical analysis was performed using one-way analysis of variance (ANOVA) and Tukey’s test.
Results: CPT-induced hepatotoxicity was characterized by significant (P < 0.001) elevations in liver and plasma levels of aspartate aminotransferase, alanine aminotransferase, alkaline phosphatase, lactate dehydrogenase, gamma-glutamyl transferase, total bilirubin, and conjugated bilirubin when compared to control. The alterations in liver redox status of CPT-treated rats were marked by significant (P < 0.001) decreases in superoxide dismutase, catalase, glutathione, and glutathione peroxidase levels with significant (P < 0.001) increases in malondialdehyde levels when compared to control. The liver of CPT-treated rat was characterized by hepatocyte necrosis. The hepatotoxic effect of CPT was significantly abrogated in a dose-dependent fashion in rats pretreated with EEIA 100 mg/kg (P < 0.05), 200 mg/kg (P < 0.01), and 400 mg/kg (P < 0.001) when compared to CPT-treated rats.
Conclusion: EEIA has potential as treatment for CPT-induced hepatotoxicity.
Materials and Methods: Fifty-four adult male albino rats randomized into nine groups (six rats in each group) were treated orally with EEIA (100, 200, and 400 mg/kg) daily for 7 days and CPT (6 mg/kg) intraperitoneally on day 5 and 7, respectively. On day 8, the rats were anesthetized; blood samples were collected and evaluated for plasma liver function markers. Liver samples were harvested and evaluated for biochemical parameters and histology.
Statistical Analysis: Data are presented as mean ± standard error of the mean (SEM). Statistical analysis was performed using one-way analysis of variance (ANOVA) and Tukey’s test.
Results: CPT-induced hepatotoxicity was characterized by significant (P < 0.001) elevations in liver and plasma levels of aspartate aminotransferase, alanine aminotransferase, alkaline phosphatase, lactate dehydrogenase, gamma-glutamyl transferase, total bilirubin, and conjugated bilirubin when compared to control. The alterations in liver redox status of CPT-treated rats were marked by significant (P < 0.001) decreases in superoxide dismutase, catalase, glutathione, and glutathione peroxidase levels with significant (P < 0.001) increases in malondialdehyde levels when compared to control. The liver of CPT-treated rat was characterized by hepatocyte necrosis. The hepatotoxic effect of CPT was significantly abrogated in a dose-dependent fashion in rats pretreated with EEIA 100 mg/kg (P < 0.05), 200 mg/kg (P < 0.01), and 400 mg/kg (P < 0.001) when compared to CPT-treated rats.
Conclusion: EEIA has potential as treatment for CPT-induced hepatotoxicity.
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Copyright
© 2020, Author(s). This open-access article is available under the Creative Commons Attribution 4.0 (CC BY 4.0) International License (https://creativecommons.org/licenses/by/4.0/), which allows for unrestricted use, distribution, and reproduction in any medium, provided that the original work is properly cited.