Protective effect of dihydromyricetin revents fatty liver through nuclear factor‑κB/p53/B‑cell lymphoma 2‑associated X protein signaling pathways in a rat model.

Dihydromyricetin is the major flavonoid in vine tea, whose pharmacological action has attracted increasing attention in recent years. The triglyceride, albumin (ALB), alanine aminotransferase, aspartate aminotransferase, malondialdehyde, superoxide dismutase, glutathione (GSH), GSH peroxidase, tumor necrosis factor‑α, interleukin (IL)‑1β, IL‑6 and IL‑18 expression levels were measured using enzyme‑linked immunosorbent assay kits. The protein levels of ALB and collagen I, PPARα, NF‑κB, p53 and Bax were used to measure using western blotting. The results revealed that dihydromyricetin prevented the development of fatty liver, and inhibited oxidative stress, inflammation and apoptosis in a fatty liver rat model. In addition, treatment with dihydromyricetin inhibited the levels of ALB and collagen I, while it induced peroxisome proliferator‑activated receptor α protein expression. Dihydromyricetin also suppressed the protein expression levels of nuclear factor (NF)‑κB, p53 and B‑cell lymphoma 2‑associated X protein (Bax) in the rat model. Collectively, it is concluded that dihydromyricetin exerted a protective effect on fatty liver through NF‑κB/p53/Bax signaling pathways in a rat model.

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