CAJ | 학술논문

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 ／mL），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 ／mL）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。
목적：관찰황금감예처리대세포조망급조망상관단백표체적영향，탐토기보호내피세포적궤제。방법취웅성 Wistar 대서흉주동맥제취내피세포，분성정상대조조、ox-LDL 자격조화황금감처리조，정상대조조용10％FBS 적 ECM 배양액배양，령외량조분별향배양액중적가불동농도적 ox-LDL 화황금감（10、25、50μg ／mL），배양24 h 후측정세포조망솔이급조망단백매상관단백（Caspase-3、Bcl-2、Bax）mRNA 적표체량。후용 ox-LDL ＋황금감（50μg ／mL）처리세포，배양24 h 후측정상술지표。결과황금감자격가명현억제내피세포조망（P ＜0．01）；여동농도 ox-LDL 자격조화정상대조조상비，황금감자격후 Bcl-2 mRNA 표체량명현승고（P ＜0．01）；Bax、Caspase-3적표체량이급 Bax／Bcl-2비치교정상대조조승고；여동농도 ox-LDL 자격조상비，ox-LDL ＋황금감자격조세포조망솔강저（P ＜0．01）。황금감자격후 Bcl-2 mRNA 적표체량승고（P ＜0．01），이 Caspase-3、Bax mRNA 적표체량강저（P ＜0．01），Bax／Bcl-2비치강저（P ＜0．01）。결론황금감예방내피세포손상적작용가능시통과증강 Bcl-2표체，감소 Caspase-3、Bax 적활화병강저 Bax／Bcl-2적비치실현적。
Objective To explore the possible mechanism of baicalin on the apoptosis of endothelial cells in the develop-ment of atherosclerosis (AS).Methods Endothelial cells were extracted from Wistar rats'thoracic aorta and divided into normal control group,baicalin treatment group,and ox-LDL treatment group.The control group was cultured with 10% FBS ECM,while the baicalin treatment group,and ox-LDL treatment group were cultured with different concen-trations of baicalin and ox-LDL (10,25,50 μg /mL)respectively for 24 hours.The apoptosis of cells was determined with flow cytometry,and expressions of Bax,Bcl-2 and Caspase-3 mRNA were measured with RT-PCR.After that, cells were treated with baicalin plus ox-LDL(50 μg /mL)for 24 hours and the above indexes were measured.Results After baicalin treatment,Bcl-2 mRNA expression increased (P <0.01),while Caspase-3,Bax mRNA and Bax/Bcl-2 ratio decreased (all P <0.01).Baicalin significantly inhibited apoptosis of endothelial cells in a concentration-depend-ent manner (P <0.01).Compared with the control group and ox-LDL group of the same concentration,cells treated with baicalin had markedly elevated expressions of Bcl-2 mRNA,Bax and Caspase-3 and Bax/Bcl-2 ratio.Compared with cells treated with ox-LDL,cells treated with baicalin plus ox-LDL had significantly reduced apoptosis rate (P <0.01).Conclusion Baicalin can prevent cell damage caused by ox-LDL by upregulating expression of Bcl-2 and downregulating expressions of Caspase-3 and Bax.