目的研究冬凌草甲素对人骨肉瘤细胞株MG-63细胞增殖抑制和凋亡诱导效应的分子机制。方法以流式细胞仪检测细胞周期变化；Western印迹检测CyclinD1、P21以及凋亡相关蛋白Survivin、Bcl-2和Bax表达的变化；TRAP-PCR-ELISA方法检测MG-63细胞端粒酶活性的变化；Z-IETD-fmk阻断试验检测Caspase-8阻断前后，冬凌草甲素对MG-63细胞凋亡影响的变化。结果冬凌草甲素增加G0/G1期MG-63细胞百分率，降低S期MG-63细胞百分率；浓度依赖性抑制MG-63细胞的CyclinD1、Survivin和Bcl-2蛋白表达，上调P21和Bax蛋白表达；浓度依赖性抑制MG-63细胞端粒酶的活性；Z-IETD-fmk阻断Caspase-8活性后，能部分逆转和减弱冬凌草甲素对MG-63细胞的凋亡诱导作用。结论冬凌草甲素通过影响细胞周期调节蛋白、阻断细胞周期G1/S期“稽查点”；抑制Survivin、Bcl-2，上调Bax；抑制端粒酶活性以及活化Caspase-8等途径抑制MG-63细胞增殖及诱导MG-63细胞凋亡。

Objective To study the molecular mechanism of oridonin in the inhibiting the proliferation and inducing apoptosis of osteosarcoma cell MG-63. Methods The change of cell cycle was analyzed by flow cytometry，the protein expression of CyclinD1，P21，and apoptosis-associated protein Survivin，Bcl-2 and Bax in MG-63 cells were detected by Western blotting method. TRAP-PCR-ELISA was applied for the detection of telomerase activities. After the activation of Caspase-8 was inhibited，the proliferation-inhibiting and apoptosis-inducing effects of Oridonin were detected by Z-IETD-fmk blocking test. Results Oridonin increased the percentage of G0 /G1 phase and decreased S phase of MG-63 cells，down-regulated CyclinD1，Survivin and Bcl-2，and up-regulated P21 and Bax protein in a concentration-dependent way in MG-63 cells. Oridonin down-regulated telomerase activities in a concentration-dependent way in MG-63 cells. The apoptosis-inducing effects of oridonin were partly suppressed after Z-IETD-fmk blocking the Caspase-8 activation of MG-63 cells. Conclusion Oridonin inhibits proliferation and induces apoptosis of MG-63 cells through regulating cell cycle protein，blocking checkpoint of G1/S phase，down-regulating Survivin and Bcl-2，up-regulating Bax and activating Caspase-8.

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