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作 者:康铁朵[1] 吕树铮[1] 王绿娅[2] 宁尚秋[1] 韩静[3] 陈韵岱[1]
机构地区:[1]首都医科大学附属安贞医院心内科 [2]北京心肺血管疾病研究所 [3]北京中医药大学
出 处:《中西医结合心脑血管病杂志》2003年第12期703-705,共3页Chinese Journal of Integrative Medicine on Cardio-Cerebrovascular Disease
基 金:北京市科委重点实验室项目 (No .953850 70 0 - 4 )
摘 要:目的 :观察葛根素促进人脐动脉血管平滑肌细胞凋亡的作用 ,探讨葛根素抑制平滑肌细胞增殖的机制。方法 :分离培养人脐动脉平滑肌细胞 ,不同浓度葛根素与细胞孵育 ,TUNEL检测葛根素诱导细胞凋亡 ,rt -PCR实验检测促凋亡基因Bax和抗凋亡基因Bcl -XL。结果 :随着葛根素浓度升高 ,细胞生长受抑制 ,TUNEL阳性细胞显著增加。rt -PCR实验发现促凋亡基因Bax随药物浓度和作用时间的增加而上升 ,而且Bax、Bcl -XL 基因表达比例有一定升高。结论 :葛根素通过调节经典的Bax、Bcl-XL 通路对血管平滑肌细胞凋亡有一定诱导作用。Objective: To discuss the mechanism of puerarin possesses the function of proliferation artery smooth muscle cell by observing it's promoting VSMC apoptosis. Methods: The VSMC derived from foetus umbilical artery, were stimulated by puerarin with different density, TUNEL was used to detect the apoptosis of artery smooth muscle cell. The promoting apoptosis gene Bax and the anti-apoptosis gene Bcl-XL were detected by RT-PCR. Results: With the Increased density of puerarin, the VSMC growth was depressed and positive cell was observed in TUNEL test. Rt-PCR test find that promoting apoptosis gene Bax increased followed elevated density of drug, and expression ratio of VSMC Bax/Bcl-XL mRNA in puerarin group was increased. Conclusion: Puerarin could induce VSMC apoptosis by classics channel of Bax?Bcl-XL
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