Protective role of resveratrol against VCM-induced hepatotoxicity in male wistar rats

Abstract

Background: Vancomycin is a glycopeptide antibiotic with a high risk of acute liver injury. Resveratrol is believed to protect the liver against toxicity.Aim: To investigate the ability of resveratrol to attenuate vancomycin-induced liver toxicity in rats injected with vancomycin.Method: Twenty-four adult male Wistar rats were distributed into three groups. The control group received only a vehicle, while the treated group received either vancomycin 200 (mg/kg, i. p.) only or vancomycin (200 mg/kg, i. p.) with resveratrol (20 mg/kg, oral gavage). All groups received their dose once daily for 7 days. Hepatic damage was assessed by measuring biochemical parameter levels in serum, aspartate transaminase (AST), alanine transaminase (ALT), alkaline phosphatase (ALP), and lactate dehydrogenase (LDH). Also, antioxidants and inflammation biomarkers such as Interleukin-6 (IL-6), malondialdehyde (MDA), nitric oxide (NO), and glutathione (GSH) were measured. Furthermore, the vancomycin-induced pathological changes in the liver were evaluated by histopathological studies.Results: In the vancomycin-treated group, hepatic serum biomarkers such as AST, ALT, ALP, IL-6, and MDA were elevated, while NO and GSH were depleted. However, resveratrol co-treatment with vancomycin prevented the elevation of AST, ALT, ALP, IL-6, and MDA and it protected the liver from NO and GSH depletion. Also, regarding vancomycin-induced degeneration of hepatocytes, resveratrol co-treatment with vancomycin prevented such degeneration and improved mononuclear cells in the liver.Conclusion: The results showed that oral administration of resveratrol has a significant hepatoprotective effect against vancomycin-induced hepatotoxicity.

Effects of Long-Term High-Ergosterol Intake on the Cholesterol and Vitamin D Biosynthetic Pathways of Rats Fed a High-Fat and High-Sucrose Diet

“…42) Hence, in this study, we used the HFHS rat model to evaluate ergosterolmediated inhibition of dyslipidemia. Additionally, HFHS diets induce hepatic damage (indicated by increasing AST, ALT, ALP, and LDH levels at 2.6-to 23.0-fold), 26,27) cholestasis (indicated by increasing ALP, T-BIL, D-BIL, I-BIL, and TBA levels at 2.5to 23.7-fold), [27][28][29][30] hypercholesterolemia (indicated by increasing T-CHO, F-CHO, and LDL-C levels at 2.5-to 6.5-fold), 17) and an increased risk of cardiovascular disease…”

“…[28][29][30] This is because studies have a reduction in ALP, T-BIL, D-BIL, and TBA levels (31%, 51%, 34%, and 39%, respectively), which play a therapeutic role in resisting cholestasis. 26,27,42) Ergosterol, brassicasterol, and vitamin D2 were detected in the HFHS + ES group, indicating that the HFHS diet with long-term ergosterol intake facilitated the absorption ergosterol, its conversion to brassicasterol by DHCR7, [9][10][11][12] and ultimately its conversion to vitamin D2 by UV light. 8) Notably, ergosterol intake significantly decreased plasma squalene and desmosterol levels and significantly increased plasma 7-dehydrocholesterol levels compared with the HFHS group.…”

Carvacrol prevents acrylamide-induced oxidative and inflammatory liver damage and dysfunction in rats

“…It has been reported that carvacrol exhibits hepatoprotective activity by increasing the total antioxidant capacity (TAS), suppressing the increase in total oxidant capacity (TOS) and MDA ( Mohseni et al, 2020 ). It has been reported that carvacrol has hepatoprotective properties by suppressing the expression of TNF-α, interleukin-6, and NF- κB ( Aristatile et al, 2013 ; Alshehri and Alorfi, 2023 ). Again, carvacrol has been documented to prevent the increase in liver function tests with ethanol ( Khan et al, 2019 ).…”