摘要
目的 :研究大蒜多糖 (GP)对中毒性心肌炎心肌细胞凋亡及Bcl -2、Bax蛋白表达的影响 ,探讨GP抑制心肌细胞凋亡的可能机制。方法 :建立小鼠阿霉素 (ADR)中毒性心肌炎模型 ,利用缺口末端标记法检测心肌凋亡细胞 ;免疫组化法检测心肌细胞bcl 2、bax基因的蛋白表达情况 ,并利用电镜观察心肌结构变化。结果 :ADR( 3mgkg-1ip ,qod× 7)可致小鼠心肌细胞凋亡数明显升高 ,心肌细胞线粒体水肿 ,促进心肌细胞凋亡蛋白bax和抑制细胞凋亡蛋白bcl 2含量均明显升高 ,但bax/ bcl- 2的比值同时升高明显 ,与正常组比较有显著差异性 (P <0 . 0 1 )。GP可逆转ADR所致的上述改变 ,表现为剂量依赖性抑制细胞凋亡 ,降低bax蛋白表达同时增加bcl 2表达 ,使bcl- 2/ bax的比值增加 (P <0 .0 5或P <0 . 0 1 )。结论 :GP能拮抗阿霉素所致的小鼠中毒性心肌炎心肌细胞凋亡作用 ,其作用机制可能与抑制Bax基因的蛋白表达 ,使Bcl -2基因表达的蛋白功能相对增强 ,Bcl -2 /Bax比值升高有关。
Objective: To investigate the effects and possible mechanism of garlic polysaccharide (GP) on cardiomyocyte apotosis and the Bcl-2, Bax gene expression on adriamycin (ADR)-induced cardiotoxicity in mice. Method: ADR was injected intraperitoneally to induce myocardium injury model in mice. The apoptotic cardiomyocyte was shown by in situ end labeling method, Bcl-2 and Bax gene expression was evaluated with immunocytochemistry. With scanning electron microscope, the cardiac ultrastructural changes were examined. Results: ADR (3mgkg -1 ip, qod(7) increased the number of apotosis cardiomyocyte. There was no significant difference in the Bcl-2 gene expression between the GP treated groups and ADR group (P>0.05), but the gene expression of Bax decreased remarkably in GP treated groups as compared with that of ADR group (P<0.05 or P<0.01). The protein expression ratio of Bcl-2/Bax increased in GP groups. Conclusion: GP has the obvious anti-apototic effect on ADR-induced cardiotoxicity by inhibiting expression of Bax gene and raising the ratio of Bcl-2/Bax.
出处
《中国生物工程杂志》
CAS
CSCD
北大核心
2005年第3期40-43,59,共5页
China Biotechnology
基金
湖北省自然基金资助项目 (2 0 0 1ABB166)
湖北省教育厅资助项目 (2 0 0 1B44 0 0 1)。
