Publication Details
Abstract
Camellia sinensis exhibits potential hepatoprotective properties attributed to its high polyphenolic content, especially catechins. This study sought to assess the efficacy of C. sinensis extract in mitigating ethanol-induced hepatic injury in a rat model, with particular emphasis on biomarkers associated with oxidative stress and inflammatory responses. Adult male of Wistar rats were allocated into four experimental groups , control, ethanol-treated (ETOH), ethanol plus low-dose C. sinensis (ETOH + CSL) and ethanol plus high-dose C. sinensis (ETOH + CSH). Hepatic damage induced by ethanol was evaluated by quantifying serum concentrations of tumor necrosis factor-alpha (TNF-α), interleukin-6 (IL-6) and malondialdehyde (MDA) as a key of oxidative stress biomarker. Ethanol exposure markedly increased TNF-α, IL-6, and MDA levels relative to the control group, indicating pronounced hepatic inflammation and oxidative stress. However, supplementation with C. sinensis extract dose-dependently reduced TNF-α and IL-6. Particularly, the high-dose C. sinensis group (ETOH + CSH) exhibited a significant reduction in both pro-inflammatory cytokines and MDA levels, emphasizing its strong role as anti-inflammatory and antioxidant. The conclusion show that C. sinensis extract, particularly at higher doses, can mitigate ethanol-induced hepatic damage by modulating inflammation and oxidative stress and these results support the potential therapeutic use of C. sinensis in treating alcoholic liver diseases.