Find in Library

Excessive alcohol intake can cause sustained or severe alcoholic liver injury (alcoholic liver disease). The purpose of this study was to explore the effect of Camellia vietnamensis active peptide (CMAP) A1-2 on alcohol-induced liver injury cells. Alcohol at 200 mmol/L reduced the survival rate of L-02 liver cells and caused a large amount of apoptosis. CMAP A1-2 component at 200 μg/mL was not toxic to normal cells and restored alcohol-induced cell survival. The main mechanisms of action of the CMAP A1-2 component included inhibiting alcohol-activated enzymes, such as alcohol-activated acetaldehyde dehydrogenase and cytochrome P4502E1, restoring glutathione content reduced by the action of alcohol, reducing intracellular reactive oxygen species level and inhibiting oxidative damage caused by ethanol. Moreover, CMAP A1-2 component activated p38 to regulate nuclear transcription factor, promote the expression of antioxidant enzyme (Hemeoxygenase-l) and protein kinase C, and reduce cell damage caused by alcohol.