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川芎嗪对花生四烯酸诱导血管内皮细胞凋亡的保护作用
引用本文:张冀,王韵,汪炳华,陈丽达,夏腊菊.川芎嗪对花生四烯酸诱导血管内皮细胞凋亡的保护作用[J].中国组织工程研究与临床康复,2003,7(30):4066-4067.
作者姓名:张冀  王韵  汪炳华  陈丽达  夏腊菊
作者单位:武汉大学医学院生物化学与分子生物学系,湖北省武汉市,430071
基金项目:湖北省教委资助项目(99A060)~~
摘    要:目的:研究川芎嗪对花生四烯酸(160μmol/L)诱导的血管内皮细胞损伤和凋亡的保护作用及其机制。方法:MTT法检测细胞存活率,比色法测LDH释放率和细胞MDA含量Hoechst33258荧光染色观察细胞核形态变化并测定凋亡率,琼脂糖凝胶电泳检测DNA降解。结果:川芎嗪(0.25~1.00mmol/L)能浓度依赖性抑制花生四烯酸引起的细胞存活率下降(t=2.52~3.14,P<0.05),并降低细胞LDH释放率和MDA含量(t=3.27~5.88和t=4.64~7.41,P<0.05)。花生四烯酸处理24h后的细胞呈现典型的凋亡核固缩表现,凝胶电泳显示DNA凋亡梯带。川芎嗪(0.25~1.00mmol/L)能降低其凋亡率。结论:川芎嗪对花生四烯酸引起的内皮细胞损伤和凋亡具有保护作用其机制可能与其抗脂质过氧化作用有关。

关 键 词:花生四烯酸  细胞凋亡  脂质过氧化作用

Protective effect of tetramethylpyrazine on apoptosis of vascular endothelial cells induced by arachidonic acid
Ji Zhang,Yun Wang,Bing Hua Wang,Li Da Chen,La Ju Xia.Protective effect of tetramethylpyrazine on apoptosis of vascular endothelial cells induced by arachidonic acid[J].Journal of Clinical Rehabilitative Tissue Engineering Research,2003,7(30):4066-4067.
Authors:Ji Zhang  Yun Wang  Bing Hua Wang  Li Da Chen  La Ju Xia
Institution:Ji Zhang,Yun Wang,Bing Hua Wang,Li Da Chen,La Ju Xia,Department of Biochemistry and Molecular Biology,Medical College,Wuhan University,Wuhan 430071,Hubei Province,China
Abstract:AIM:To study the protective effects and mechanism of Ligustrazine against damage and apoptosis in human umbilical vascular endothelial cells(HUVECs) induced by 160 μ mol/L arachidonic acid(AA). METHODS:The survival rate of cells was detected by MTT,the release rate of lactate dehydrogenase(LDH) and malondialdehyde(MDA)content in endothelial cells(EC) are measured by colorimetric assay.Hoechst 33258 fluorescence staining was used to observe morphological changes of nucleus and determine apoptotic ratio.Agarose gel electrophoresis was used to detect DNA fragmentation. RESULTS:MP(0.25- 1.0 mmol/L) prevented the inhibitory effect of viability induced by AA(t=2.52- 3.14,P< 0.05).TMP(0.25- 1.0 mmol/L) partly prevented the increase in the release rate of LDH and MDA contents induced by AA(t=3.27- 5.88,t=4.64- 7.41,P< 0.05).Cells treated with 160 μ mol/L AA showed typical morphological changes of apoptosis.A " DNA ladder" was also observed.TMP(0.25- 1.0 mmol/L) partly decreased the ratio of apoptotic cells. CONCLUSION:TMP can protect AA induced apoptosis in EC and the mechanism of its action may be related to anti lipid peroxidation.
Keywords:TMP can protect AA  induced apoptosis in EC and the mechanism of its action may be related to anti  lipid peroxidation    
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