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作 者:张苗[1] 李春仁[1] 芦茜[1] 陈硕[1] 王新全[1] 周林[1] 曾春雨[1]
机构地区:[1]第三军医大学大坪医院野战外科研究所心血管内科、重庆市心血管病研究所,重庆400042
出 处:《第三军医大学学报》2015年第5期404-408,共5页Journal of Third Military Medical University
基 金:国家重点基础研究发展计划(973计划,2012CB517801)~~
摘 要:目的探讨细颗粒物(fine particulate matter,PM2.5)对SD大鼠心肌梗死(myocardial infraction,MI)的影响及心肌组织中Mitsugumin 53(MG53)蛋白表达的变化。方法将40只体质量210~250 g的雄性SD大鼠分为假手术(Sham)组、MI组、Sham+PM2.5组、MI+PM2.5组(n=10)。通过结扎左冠状动脉前降支建立心肌梗死模型。Sham+PM2.5组及MI+PM2.5组经气道滴灌PM2.5混悬液(10 mg/m L,40μL/次,3次/周,共4周),Sham组及MI组同法滴灌等量PBS缓冲液作为对照。4周后观察各组大鼠肺组织病理变化、心肌梗死面积、心功能情况、大鼠生存率及心肌组织中MG53蛋白表达的变化。结果 HE染色显示气道滴灌PM2.5的大鼠肺组织可见细颗粒物沉积,表明滴灌成功。MI+PM2.5组与MI组大鼠相比,4周后心肌梗死面积明显增大[(17.78±2.13)%vs(11.49±2.23)%,P〈0.05],射血分数(EF%)显著降低[(37.14±5.14)%vs(47.13±4.09)%,P〈0.05],生存率下降,心肌梗死区MG53蛋白的表达也明显降低。结论 PM2.5会加重大鼠心肌梗死的程度,其原因可能与PM2.5抑制心肌受损的膜修复因子MG53蛋白的表达有关。Objective To determine the effect of fine particulate matter( PM2. 5) on myocardial infarction( MI) and the protein expression of mitsugumin 53( MG53) in infracted heart of SD rats. Methods Forty male SD rats( 210 to 250 g) were randomly divided into sham-operated group,MI group,sham +PM2. 5group,and MI + PM2. 5group( n = 10 in each group). The rats were subjected to ligate the left anterior descending coronary artery to establish the MI model. For sham + PM2. 5group and MI + PM2. 5group,PM2. 5suspension was administered by intra-tracheal instillation at a dose of 10 mg / m L,each time 40 μL,3 times a week for 4 weeks,and the other 2 groups were exposed to equal volume of phosphate-buffered saline( PBS).In 4 weeks after instillation,the pathological changes in lung tissue,MI size,cardiac function,survival rate,and the protein level of MG53 in the myocardial tissue were observed and detected respectively. Results HE staining revealed PM2. 5deposition in the lung tissue in the rats receiving PM2. 5suspension instillation,which indicated that our operation was successful. Compared with MI group,the MI + PM2. 5group had evidently larger infract size [( 17. 78 ± 2. 13) % vs( 11. 49 ± 2. 23) %,P 0. 05 ],decreased ejection fraction [EF%,( 37. 14 ± 5. 14) % vs( 47. 13 ± 4. 09) %,P 0. 05 ],reduced overall survival rate,and lowered expression of MG53 protein. Conclusion PM2. 5significantly enhances the degree of MI,which might be due to its inhibition on the expression of MG53 protein which is myocardial damaged membrane repair factor.
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