摘要
目的 研究人参皂甙Re对急性缺血再灌注心肌细胞凋亡及fas基因表达的影响 ,探讨人参皂甙Re抑制缺血再灌注心肌细胞凋亡的分子机制。方法 结扎Wistar大鼠左冠状动脉前降支 (LAD) ,建立大鼠急性缺血再灌注动物模型。 30只大鼠分 3组 (每组 10只 ) :人参皂甙Re组 ,缺血再灌注组和假手术组。用透射电镜和TUNEL法检测心肌细胞凋亡 ,并用光学显微镜进行凋亡细胞计数 ,免疫组化法检测Fas蛋白表达 ,利用图像分析系统检测阳性结果的平均吸光度 (A)值进行定量分析。结果 心肌细胞的凋亡数在缺血再灌注组、假手术组和人参皂甙Re治疗组每视野分别为 134 4 5± 4 5 6 1、 0 18± 0 0 9和 90 6 6± 19 2 2 ,各组间的心肌细胞凋亡数有显著差异 (P <0 0 5 )。缺血再灌注组、假手术组和人参皂甙Re治疗组的Fas蛋白的平均A值分别为 :0 13± 0 0 3、 0 0 6± 0 0 1和 0 0 7± 0 0 1,人参皂甙Re治疗组与缺血再灌注组相比差异有显著性意义 (P <0 0 5 )。结论 人参皂甙Re能显著抗急性缺血再灌注损伤诱导的心肌细胞凋亡 ,抑制急性缺血再灌注诱导心肌细胞内Fas蛋白表达可能是作用机制之一。
Objective To study the effects of Ginsenoside Re on cardiomyocyte apoptosis following acute ischemia-reperfusion in vivo and fas gene expression and explore the molecular mechanism of Ginsenoside Re inhibiting cardiomyocyte apoptosis induced by acute ischemia-reperfusion injury. Methods The left anterior descending artery in Wister rats was ligated to establish an acute ischemia-reperfusion model. Thirty animals were equally divided into 3 groups (n=10 in each group): Ginsenoside Re treated group, acute ischemia-reperfusion (I/R) group and sham-operated group. The apoptosis of the cardiomyocytes was determined by TUNEL staining and observed under transmission electron microscopy. The numbers of apoptotic cells were counted by optic microscopy. Immunohistochemistry was used to detect 0.18±0.09 the expression of Fas protein in the cardiomyocytes. Image processing system was used to quantitatively estimate the positive metric substances of immunohistochemistry through the average absorbance value. Results The number of the apoptotic cells were 134.45±45.61 (I/R group), 0.18±0.09 (sham operated group) and 90.66±19.22 (Ginsenoside Re treated group) in each visual field respectively with the difference being significant (P<0.05). Fas gene expression was decreased very significantly in Ginsenoside Re treated group as compared with that in the I/R group (0.07±0.01 vs 0.13±0.03, P<0.05). Conclusion Ginsenoside Re could inhibit cardiomyocyte apoptosis induced by acute ischemia and reperfusion injury; One of the mechanisms might be that Fas protein expression following acute ischemia and reperfusion was inhibited.
出处
《华中科技大学学报(医学版)》
CAS
CSCD
北大核心
2004年第3期286-288,共3页
Acta Medicinae Universitatis Scientiae et Technologiae Huazhong
基金
湖北省自然科学基金资助项目 (No 2 0 0 0J0 5 0 )