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机构地区:[1]南京医科大学附属南京医院南京市第一医院内分泌科,江苏南京210000 [2]南京医科大学附属南京医院南京市第一医院普外科,江苏南京210000
出 处:《临床荟萃》2014年第1期45-48,F0003,共5页Clinical Focus
基 金:南京市医学科技发展项目(ZKX12023)
摘 要:目的格雷夫斯病(Graves disease,GD)患者肝功能损害发病率高,可能与升高的促甲状腺激素受体抗体(TRAb)相关,探讨TRAb对肝细胞损伤的机制。方法用含不同浓度TRAb的GD患者血清、正常人血清及胎牛血清的DMEM培养基处理人肝癌细胞株HepG2细胞,采用异硫氰酸荧光素(annexin V-FITC)/碘化丙啶(propidium iodide,PI)及MTT法分别检测细胞的凋亡和增殖状况。结果 5%、10%及20%TRAb的GD血清能促进HepG2细胞增殖,且HepG2细胞凋亡较对照组增高明显,以中晚期凋亡为著。结论 TRAb能诱导人肝癌细胞HepG2细胞凋亡,参与肝细胞损伤的发生。Objective Patients with Graves disease(GD) have a high prevalence of hepatic dysfunction,which may be related to elevated thyrotropin receptor antibody(TRAb). The study was designed to investigate the possible mechanism of TRAb induced hepatic dysfunction. Methods Human hepatoma HepG2 ceils were treated with different serum concentrations of GD patients, healthy controls and fatal bovine serum(FBS). The cell apoptosis and proliferation of HepG2 cells were analyzed by annexin V-FITC/PI and MTT, respectively. Results 5 %, 10% and 20 % serum of GD promoted the proliferation of HepG2. The apoptosis rates of GD serum were higher than those of normal and FBS controls,in which both interim and late apoptosis were significant. Conclusion TRAb can induce apoptosis in HepG2 cells ,which may contribute to the hepatic dysfunction.
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