摘要
目的:研究D-木糖(D-xylose)对酒精诱导的肝细胞发生脂肪性变的保护作用.方法:用酒精诱导肝HepG2细胞株损伤,设立正常对照组、酒精损伤组和不同浓度的D-木糖保护组;形态学观察细胞凋亡以及生长情况,以MTT法检测细胞存活力,通过油红O染色对存活细胞脂变程度进行观察并量化比较,RT-PCR检测PPARγ水平的变化,综合评价酒精引起细胞脂肪性病变的机制.结果:肝HepG2细胞经酒精损伤后,可见细胞形态肿胀变形或萎缩,出现凋亡小体,细胞数量明显降低,脂肪变程度严重.经不同浓度D-木糖给药处理,各保护组的肝脏细胞存活率显著升高(88.5%、81.8%、75.4%vs44.0%,P<0.05);脂变程度明显减轻(0.63250±0.068172、0.60400±0.042798、0.95538±0.067853vs0.97313±0.063481,P<0.05);同时,酒精损伤组PPARγ的mRNA表达水平较正常对照组有明显提高,而D-木糖保护组中其表达量降低,以高浓度组最为显著.结论:D-木糖可降低酒精对肝细胞的损伤作用,降低细胞脂变程度,可能是通过降低脂肪生成的速度而实现的.
AIM： To investigate the protective effect of D-xylose against alcohol-induced hepatic cell steatosis. METHODS： HepG2 cells were divided into three groups： normal control group, alcohol- injured group, and D-xylose group. Steatosis was induced with alcohol in cells in the alcohol- injured group and D-xylose group. The D-xylose group was treated with different concentrations of D-xylose. After treatment, cell apoptosis and growth were observed based on morphology, while cell viability was tested by MTT assay. The degree of steatosis in viable cells was evaluated by Oil Red O staining. RT-PCR was employed for testing the changes in PPAR7 expression levels. RESULTS： In the D-xylose groups, hepatic cell survival rate was increased significantly （88.5%, 81.8%, 75.4% vs 44.0%, all P 〈 0.05） andthe degree of steatosis was alleviated （0.63250 ± 0.068172, 0.60400 ± 0.042798, 0.95538 ± 0.067853 vs 0.97313 ± 0.063481, all P 〈 0.05） compared to the alcohol-injured group. The mRNA level of PPARy was significantly higher in the alcohol- injured group than in the control group; howev- er, D-xylose significantly reduced the degree of steatosis in a concentration-dependent manner. CONCLUSION： D-xylose can reduce alcohol- induced hepatic cell injury and steatosis possibly by decreasing lipid generation.
出处
《世界华人消化杂志》
CAS
北大核心
2012年第24期2259-2264,共6页
World Chinese Journal of Digestology
