高剂量O-糖基化修饰抑制剂Benzyl-α-GalNAc诱导体外培养肝细胞脂肪变  

Effect of O-Glycosylation Inhibitor, Benzyl-α-GalNAc, on Hepato- cytes in vitro

作　　者：张晓静[1] 张仁雯[1] 郝晓花[2] 任慧[2] 李红敏[2] 刘燃[2] 王智强[1] 魏红山[1,2] 

机构地区：[1]北京大学地坛医院教学医院北京大学医学部,北京市100015 [2]首都医科大学传染病研究所首都医科大学附属北京地坛医院,北京市100015

出　　处：《医学分子生物学杂志》2013年第5期259-263,共5页Journal of Medical Molecular Biology

基　　金：国家自然科学基金（No.81071411,81271901）

摘　　要：目的初步探讨蛋白质O-糖基化抑制剂Benzyl-α-GalNAc对肝细胞的影响。方法取雌性Balb／c小鼠（8～10周）20只随机分为正常组（n=10），Benzyl—d—GalNAc药物组（n=10），给Benzyl-α-GalNAc药物（5mg／kg，1次／d）灌胃。第2周末取小鼠血清及肝脏进行血清生化指标AIJT及AlJP测定及肝组织HE染色。培养HepG2细胞．Benzyl-α-GalNAc分别以0．5、1及5mg／ml与HepG2细胞共孵育。24h后进行油红O染液染色。5mg／ml药物组完全未贴壁，去除处理因素，继续培养12h观察细胞。Benzyl-α-Gal—NAc以3mg／ml处理HepG2细胞12h及24h观察细胞贴壁情况。培养L02细胞，Benzyl-α-GalNAc分别以0．1及0．5mg／ml与L02细胞共孵育。24h后进行油红O染液染色。结果药物组与正常对照组比较，肝组织切片显示轻微脂肪变。油红O染色显示药物处理组HepG2及L02细胞内的脂滴积聚。高浓度组细胞完全没有贴壁，24h后更换无药物培养基，去除处理因素12h后，可见HepG2开始贴壁生长。结论高浓度O-糖基化抑制剂Benzyl-α-GalNAc抑制体外肝细胞的黏附，并诱导轻微肝细胞脂肪变。Objective To investigate the high concentration of the potential tion inhibitor, Benzyl-α-GalNAc, on the function of the liver cell Methods role of O-glycosyla- Femal Balb/c mice （8-10 weeks old） were randomly divided into two groups; Control group （C, n = 10）, Benzyl-α- GalNAc treated group （ D = 10） . Benzyl-ot-GalNAc group was treated by Benzyl-α-GalNAc （5 mg/ kg ） once a day. At the second week, serum and liver tissues of mice were collected. HepG2 cells were treated by Benzyl-α-GalNAc at 0. 5 mg/ml , 1 mg/ml and 5 mg/ml, respectively. After 24 h the HepG2 cells were stained with oil red O. Removed processing factor, Benzyl-α-GalNAc treated HepG2 cells were continue to culture 12 h. Benzyl-α-GalNAc treated HepG2 cells with 3 mg/ml observing at 12 h and 24 h. L02 cells were treated by Benzyl-α-GalNAc at 0. 1 mg/ml , 0. 5 mg/ml, respectively. After 24 h the LO2 cells were stained with oil red O. Results The mild fatty injury of liver tissue in Benzyl-α-GalNAc treated mice, compared with those of control mice. HepG2 cells of control was completely adherence after cultured 12 h, but the Benzyl-α-GalNAc-treated HepG2 cells were completely not adherence. After removed processing factor, and continued to culture 12 h, the HepG2 cells re-adherenced. Compared with control mice, there was no significant variation of biochemical maker in Benzyl-α-GalNAc treated mice. Conclusion High concentration of O-glycosylation inhibitor, Benzyl-α-GalNAc, could induce fatty liver inury in vivo. and inhibit the adherence of cells in vitro.

关 键 词：O-糖基化修饰抑制剂 Benzyl-α-GalNAc 肝细胞脂肪变 黏附 

分 类 号：R313[医药卫生—基础医学]