ABSTRACT

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.

摘要

过量饮酒会导致持续或严重的酒精性肝损伤（酒精性肝病）。本研究的目的是探讨越南茶花的功效。活性肽 (CMAP) A1-2 对酒精性肝损伤细胞的影响。200 mmol/L 的酒精会降低 L-02 肝细胞的存活率并导致大量细胞凋亡。200 μg/mL 的 CMAP A1-2 组分对正常细胞无毒，并恢复酒精诱导的细胞存活。CMAP A1-2成分的主要作用机制包括抑制酒精活化酶，如酒精活化乙醛脱氢酶和细胞色素P4502E1，恢复因酒精作用而降低的谷胱甘肽含量，降低细胞内活性氧水平，抑制氧化损伤。乙醇引起的。此外，CMAP A1-2成分激活p38以调节核转录因子，促进抗氧化酶（Hemeoxygenase-l）和蛋白激酶C的表达，减少酒精引起的细胞损伤。