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NS-398诱导肝癌细胞HepG2凋亡的作用机制 被引量:3

The effect and possible mechanism of selective cyclooxygenase-2 inhibitor NS-398 on apoptosis in HepG2
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摘要 目的探讨NS-398诱导肝癌细胞HepG2凋亡的分子机制。方法采用MTT法测定COX-2选择性抑制剂NS-398对HepG2细胞的增殖抑制率;流式细胞仪检测凋亡;原位细胞凋亡检测法观察细胞凋亡形态学变化;免疫细胞化学分析COX-2、cIAP-1、XIAP、Survivin蛋白变化。结果 NS-398对HepG2细胞株有增殖抑制作用,流式细胞仪检测用药组凋亡率明显高于对照组。TUNEL染色可见典型的凋亡形态学特征。免疫细胞化学分析表明使用NS-398后,COX-2、cIAP-1、XIAP、Survivin蛋白表达降低。结论 COX-2选择性抑制剂NS-398对人肝癌细胞株HepG2有诱导凋亡作用,其机制可能通过抑制COX-2,下调cIAP-1、XIAP、Survivin的表达而诱导凋亡。 Objective To explore the effect of selective cyclooxygenase-2 inhibitor NS-398 on apoptosis in HepG2 and possible mechanism. Methods The inhibitor effect of NS-398 on HepG2 cell lines was measured by MTT assay. The apoptosis rate was deteceted by flow cytometry and the morphological change of apoptosis was observed by TUNEL. The expression of COX-2,cIAP-1,XIAP,Survivin were assayed by immunohistochemical staining. Results NS-398 had anti-proliferative effect on HepG2 cell lines. The cells showed distinctive apoptotic characteristics by TUNEL and the apoptosis rate which treated with NS-398 was higher than control group. The expression of COX-2, cIAP-1,XIAP,Survivin were decreased. Conclusion NS-398 can inhibit the proliferation and increase apoptosis in human HepG2 cells lines. The possible mechanism is downregulate the expression of COX-2,cIAP-1,XIAP to induce apoptosis.
出处 《安徽医科大学学报》 CAS 北大核心 2010年第5期655-659,共5页 Acta Universitatis Medicinalis Anhui
基金 国家自然科学基金资助项目(编号:30772537)
关键词 肝细胞 细胞凋亡 环氧化酶2 carcinoma hepatocellular apoptosis cyclooxygenase-2
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