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目的观察黄芩苷预处理对细胞凋亡及凋亡相关蛋白表达的影响,探讨其保护内皮细胞的机制。方法取雄性Wistar大鼠胸主动脉提取内皮细胞,分成正常对照组、ox-LDL刺激组和黄芩苷处理组,正常对照组用10%FBS的ECM培养液培养,另外两组分别向培养液中滴加不同浓度的ox-LDL和黄芩苷(10、25、50μg/m L),培养24 h后测定细胞凋亡率以及凋亡蛋白酶相关蛋白(Caspase-3、Bcl-2、Bax)mRNA的表达量。后用ox-LDL+黄芩苷(50μg/m L)处理细胞,培养24 h后测定上述指标。结果黄芩苷刺激可明显抑制内皮细胞凋亡(P<0.01);与同浓度ox-LDL刺激组和正常对照组相比,黄芩苷刺激后Bcl-2 mRNA表达量明显升高(P<0.01);Bax、Caspase-3的表达量以及Bax/Bcl-2比值较正常对照组升高;与同浓度ox-LDL刺激组相比,ox-LDL+黄芩苷刺激组细胞凋亡率降低(P<0.01)。黄芩苷刺激后Bcl-2 mRNA的表达量升高(P<0.01),而Caspase-3、Bax mRNA的表达量降低(P<0.01),Bax/Bcl-2比值降低(P<0.01)。结论黄芩苷预防内皮细胞损伤的作用可能是通过增强Bcl-2表达,减少Caspase-3、Bax的活化并降低Bax/Bcl-2的比值实现的。
Objective To observe the effects of baicalin preconditioning on the apoptosis and the expression of apoptosis related proteins and to explore the mechanism of its protection on endothelial cells. Methods The endothelial cells were extracted from the thoracic aorta of male Wistar rats and divided into normal control group, ox-LDL stimulation group and baicalin treatment group. The normal control group was cultured in 10% FBS ECM medium. The other two groups were respectively cultured in medium The concentrations of ox-LDL and baicalin (10, 25 and 50 μg / ml) were added dropwise and the apoptosis rate and the expression of caspase-3, Bcl-2 and Bax mRNA The amount of expression. The cells were treated with ox-LDL + baicalin (50μg / ml), and the above parameters were measured after 24h culture. Results Baicalin could significantly inhibit the apoptosis of endothelial cells (P <0.01). Compared with the same concentration of ox-LDL stimulation group and normal control group, the expression of Bcl-2 mRNA was significantly increased after baicalin stimulation (P <0.01) ; The expression of Bax, Caspase-3 and the ratio of Bax / Bcl-2 in the ox-LDL + baicalin group were significantly lower than those in the normal control group (P <0.01) ). The expression of Bcl-2 mRNA increased (P <0.01), while the expression of Caspase-3 and Bax mRNA decreased (P <0.01) and the ratio of Bax / Bcl-2 decreased after baicalin stimulation (P <0.01). Conclusion Baicalin can prevent the injury of endothelial cells by enhancing the expression of Bcl-2, decreasing the activation of Caspase-3, Bax and decreasing the ratio of Bax / Bcl-2.