| 李丽,陶辉宇,陈杰斌,邓晖,吕建华,李双杰.黄芪甲甙保护阿霉素心肌损伤大鼠抗凋亡作用的机制研究[J].中国中西医结合杂志,2006,(11):1011-1014 |
| 黄芪甲甙保护阿霉素心肌损伤大鼠抗凋亡作用的机制研究 |
| Anti-apoptosis Effect of Astragaloside on Adriamycin Induced Rat’s Cardiotoxicity |
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| DOI： |
| 中文关键词: 黄芪甲甙 阿霉素 心肌细胞凋亡 bcl-2基因 bax基因 |
| 英文关键词:astragaloside adriamycin myocardial cell apoptosis bcl-2 bax |
| 基金项目:国家自然科学研究基金项目(No.C03050402) |
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| 中文摘要: |
| 目的探讨黄芪甲甙(简称黄芪)抗阿霉素所致心肌细胞凋亡的可能机制。方法取SD大鼠随机分为空白组、模型组、黄芪3个剂量(低、中、高)组。空白组腹腔注射生理盐水,余4组分别给予阿霉素造模(15mg/kg,隔日腹腔注射1次,共6次)。黄芪3个剂量组同时用不同剂量黄芪甲甙灌胃治疗,空白组和模型组同时给予羧甲基纤维素钠。采用原位缺口末端标记法(TUNEL)检测心肌细胞凋亡,细胞免疫组织化学检测bcl-2、bax蛋白的表达;逆转录聚合酶链反应(RT-PCR)检测bcl-2、bax基因的表达。结果与空白组比较,模型组大鼠心肌细胞凋亡发生率增高(P<0·01),抑制凋亡因子bcl-2基因及蛋白表达下降(P<0·01),而促进凋亡因子bax基因及蛋白表达增强(P<0·01),bcl-2/bax mRNA比值降低(P<0·05)。与模型组比较,黄芪高剂量组大鼠心肌细胞的凋亡率显著下降(P<0·05),bcl-2基因及蛋白水平表达增强(P<0·05),bax基因及蛋白水平表达下降(P<0·05),bcl-2/bax mRNA比值明显上升(P<0·05)。结论高剂量黄芪甲甙治疗可以抑制阿霉素所致大鼠心肌细胞凋亡,其作用机制可能与凋亡基因bcl-2表达有关。 |
| 英文摘要: |
| ObjectiveTo study the possible mechanism of anti-myocardial cell apoptosis of astragaloside induced by adriamycin (ADR). Methods Fifty SD rats were randomized into five groups: the normal control group,the model group,the astragaloside low dose (A-L) group,the astragaloside medium dose (A-M) group and the astragaloside high dose (A-H) group, 10 in each group. The normal control group was given normal saline by intraperitoneal injection,while the other four groups were given ADR by intraperitoneal injection once every other day for six times with the total dosage of 15mg/kg. At the same time, different dosage of astragaloside was administrated by gavage to the three treated groups, and sodium carboxymethycellulose (SCMC) was given to the normal control and the model group. Myocardial cell apoptosis was examined by in situ end-labeled DNA (TUNEL), protein and mRNA expressions of bax, bcl-2 were detected respectively with immunohistochemistry assay and RT-PCR. Results Compared with those in the normal control, apoptosis index was significantly higher, the protein and mRNA expressions of bcl-2 were lower and those of bax were higher, in the model group, resulted in lower ratio of bcl-2/bax (P<0.05 or P<0.01). However, in the A-H group, apoptosis index decreased significantly, the expressions of bcl-2 were higher, those of bax were lower, and ratio of the bcl-2/bax increased (all P<0.05). Conclusion High dose of astragaloside could suppress the myocardial cell apoptosis induced by ADR with the possible mechanism related to regulating the expressions of bcl-2 and bax. |
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