调控内源性大麻素系统对酒精性肝细胞损伤模型的影响

The Effects of Endocannabinoid System on Alcohol-induced Liver Cell Injury

目的探索调控内源性大麻素系统对酒精诱导肝细胞损伤模型的影响.方法采用CCK-8法筛选适宜酒精浓度,建立酒精诱导的L-02人肝脏细胞和Hep G2人肝癌细胞损伤模型;筛选对细胞活性无影响的URB937浓度范围;应用酒精性肝细胞损伤模型,评估URB937对酒精损伤下肝细胞的影响.结果 0.1-50μmol/L浓度范围内,URB937对L-02和Hep G2细胞的增殖活性无抑制作用（P〉0.05）;相同浓度范围的URB937合并酒精（100 mmol/L或500 mmol/L）处理,增殖活性抑制显著,酒精诱导的细胞损伤加重,部分细胞出现坏死（P〈0.05）.结论升高内源性大麻素水平将加重酒精诱导的细胞损伤.

Objective To explore the effects of endocannabinoid system on alcohol- induced liver cell injury.Me thods Alcohol- induced liver cell injury model was established by incubating human liver cell（L- 02） and human hepatoma cell（Hep G2） with the medium containing alcohol. We screened URB937 concentration range,and evaluated its effecst on alcohol- induced liver cell injury. Re s ults Treatment with URB937（0.1 -50μmol/L） alone didn＇t affect L- 02 and Hep G2 cell viability（P〉0.05）. Under the situation of alcohol- induced liver cell injury, URB937 co- treatment induced significant cell death and necrosis（P〈0.05）. Conclus ions Elevation of endogenous anandamide concentration would aggravate the cell injury induced by alcohol.