| 袁凌燕,张红旗,徐丹令,王克强,邹云增,贾剑国,李冰玉,郝颖.通心络超微粉对血管紧张素Ⅱ引起的肾脏损伤的保护作用研究[J].中国中西医结合杂志,2009,(12):1104-1109 |
| 通心络超微粉对血管紧张素Ⅱ引起的肾脏损伤的保护作用研究 |
| Protective Effect of Tongxinluo Superfines on AngiotensinⅡCaused Renal Injury in Rat |
| 免费下载全文 查看/发表评论 下载PDF阅读器 |
| |
| DOI： |
| 中文关键词: 血管紧张素Ⅱ 肾脏损伤 氧化 凋亡 通心络 |
| 英文关键词:angiotensinⅡ renal injury oxidation apoptosis Tongxinluo |
| 基金项目:重点基础研究发展计划(973计划)资助项目(No.2005CB523302,No.2006CB503803) |
|
| 摘要点击次数: 1254 |
| 全文下载次数: 4 |
| 中文摘要: |
| 目的探讨通心络对肾脏的保护作用及作用机制。方法8周龄SD大鼠皮下埋置微量泵,缓慢释放200 ng/(kg.min)的血管紧张素Ⅱ(AngiotensinⅡ,AngⅡ),模拟病理状态下AngⅡ增高所致的肾脏组织损伤。实验分成假手术组、模型组和通心络组,每组6只。假手术组仅在背部埋置生理盐水缓释泵,通心络组用通心络超微粉灌胃(剂量每天0.8 g/kg)。14天后采用透射电镜观察肾动脉内皮形态,苏木精-伊红(HE)染色观察肾脏病理结构,以脱氧核苷酸转移酶介导的缺口末端标记(TUNEL)染色观察肾脏细胞凋亡情况,反转录聚合酶链式反应(RT-PCR)技术观察肾脏尼克酰胺腺嘌呤二核苷酸(NADPH)亚型p22phox、p53的表达及检测肾脏活性氧(reactie oxidatie species,ROS)水平。结果在AngⅡ模型中,肾动脉内皮细胞不同程度的充血、肿胀、剥脱。模型组肾小球基质增生,部分肾小球萎缩,有纤维化倾向,肾实质细胞凋亡增加,p53及p22phox表达亦增强,活性氧增加。通心络组内皮损伤减轻,通心络可减轻肾小球损伤,减少肾脏细胞凋亡,减弱p53及p22phox表达及活性氧的生成。结论通心络减轻AngⅡ所致肾脏损伤可能通过减轻肾脏血管损伤及NADPH氧化/p53通路,抑制肾实质细胞凋亡而得以实现。 |
| 英文摘要: |
| Objective To explore the renal protective effect of Tongxinluo(TXL) and its mechanism of action.Methods Eight-week old SD rats were divided into the sham-operated group(A),the model group(B) and the TXL group,6 rats in each group.Angiotensin Ⅱ(AngⅡ) was administered slowly(200 ng/kg per min) to rats in group B and C via subcutaneously embedded osmotic pump to make them simulative model of renal injury,while to rats in group A,pump embedding with saline infusion.After modeling,TXL was given to group C by gastric perfusion in dosage of 0.8 g/kg per day.And the following indexes were observed 14 days later: configuration of renal arterial endothelium by transmission electron microscope;pathologic figure of kidney with HE stain;renal apoptosis by TUNEL;expression of p53 and p22phox by RT-PCR;and level of reactive oxygen species(ROS) in kidney.Results Different degree of congestion,swelling,denudation of endothelial cell in renal arterial endothelial cell;glomerular matrix proliferation and partial glomerular atrophy with tendency of fibrosis;increased renal parenchymal apoptosis;enhanced expression of p53 and p22phox;and elevated ROS were found in model animals.All the above-mentioned abnormalities,including glomerular injury,renal cell apoptosis,as well as the increased p53,p22phox expressions and ROS production were all alleviated in group C after TXL treatment.Conclusion TXL could protect renal against AngⅡ injury,and it may be realized by inhibiting NADPH-ROS/p53 pathways and suppressing cell apoptosis in renal parenchyma. |
| 关闭 |
|
|
|
扫描微信二维码，获取更多信息