Black tea extract exerts a protective effect on diethylnitrosamine-induced hepatic precancerous lesions through the...

To investigate the protective effect and mechanism of black tea (BT) extract on diethylnitrosamine (DEN)-induced liver precancerous lesions in rats.

Fifty male Sprague-Dawley (SD) rats were randomly assigned to five groups: normal control, DEN model, and three black tea extract groups (low, medium, and high dose: DEN+BT-L, DEN+BT-M, DEN+BT-H). The model and treatment groups received DEN (50 mg/kg, i.p.) for 14 weeks, and black tea extract (25, 50, or 100 mg/kg) was administered via gavage. Liver histopathology was evaluated by hematoxylin-eosin (HE) and Masson staining. Serum levels of alanine aminotransferase (ALT), aspartate aminotransferase (AST), alkaline phosphatase (ALP), alpha-fetoprotein (AFP), interleukin-6 (IL-6), and tumor necrosis factor-alpha (TNF-α) were assessed. Hepatic oxidative stress markers-reactive oxygen species (ROS), superoxide dismutase (SOD), glutathione (GSH), and malondialdehyde (MDA)-were measured. Expression of nuclear factor erythroid 2-related factor 2 (Nrf2), heme oxygenase-1 (HO-1), NAD(P)H quinone dehydrogenase 1 (NQO1), signal transducer and activator of transcription 3 (STAT3), phosphorylated STAT3 (p-STAT3), nuclear factor-kappa B (p65), and phosphorylated p65 (p-p65) was evaluated by Western blot.

Black tea extract alleviated DEN-induced hepatocyte damage, fibrosis, and inflammation. It reduced serum ALT, AST, ALP, AFP, IL-6, and TNF-α levels, decreased ROS and MDA, and increased SOD and GSH levels in a dose-dependent manner (P < 0.05). Nrf2 and HO-1 protein levels were upregulated, while STAT3, p-STAT3, p65, and p-p65 expressions were downregulated. NQO1 expression showed a decreasing trend.

Black tea extract protects against DEN-induced liver precancerous changes by enhancing antioxidant capacity via the Nrf2/HO-1 pathway and inhibiting the NF-κB/STAT3 axis, suggesting its potential in preventing liver carcinogenesis.