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
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摘要: [摘要]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HepG2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 0.1~50 μmol/L浓度范围内,URB937对L-02和HepG2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.Abstract: [Abstract]Objective To explore the effects of endocannabinoid system on alcohol-induced liver cell injury. Methods Alcohol-induced liver cell injury model was established by incubating human liver cell(L-02)and human hepatoma cell(HepG2)with the medium containing alcohol. We screened URB937 concentration range, and evaluated its effecst on alcohol-induced liver cell injury. Results Treatment with URB937(0.1~50 μmol/L) alone didn’t affect L-02 and HepG2 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). Conclusions Elevation of endogenous anandamide concentration would aggravate the cell injury induced by alcohol.
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