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机构地区:[1]哈尔滨医科大学附属第二医院心外科,哈尔滨150086 [2]哈尔滨医科大学克山病研究所
出 处:《中国地方病防治》2004年第4期196-199,共4页Chinese Journal of Control of Endemic Diseases
基 金:国家自然科学基金课题 (39670 650 );卫生部科学研究基金 96 - 1 - 3
摘 要:目的 探讨低硒小鼠病毒性心肌炎与细胞凋亡的关系。方法 应用低硒和常硒合成饲料喂养 5周龄BALB/C雄性小鼠 5周后 ,经腹腔接种柯萨奇B3m病毒 (CVB3m) 10 3 TCD50 0 .1ml,建立小鼠心肌炎模型。对照组腹腔注射PRM164 0。通过此模型 ,采用原位末端标记法 (TUNEL法 )测定心肌凋亡细胞 ,并采用免疫组化法测定凋亡相关基因C -myc、Bcl -2及相关因子TGF -β1的表达。结果 光镜下低硒病毒组 (Ⅰ组 ) ,常硒病毒组 (Ⅱ组 )病变检出率分别为 75 %和 3 5 % ,常硒对照组 (Ⅲ组 )为 0 ,经 χ2 检验Ⅰ组显著高于Ⅱ组 (P <0 .0 5 )。对低硒及常硒病毒组的心肌采用TUNEL法检测发现凋亡细胞 ,Ⅰ组小鼠心肌中有凋亡者占 75 % ,Ⅱ组有凋亡者占 5 5 % ,Ⅲ组未见凋亡细胞。采用免疫组化法检测发现 ,Ⅰ组鼠心肌中可见C -myc和TGF -β1的阳性表达 ,分布区域与TUNEL法标记的凋亡细胞一致。Ⅲ组心肌中可见BCL -2基因表达产物 ,而Ⅰ、Ⅱ组中很少见。结论 本实验结果提示低硒能促进病毒感染引起的心肌细胞凋亡 ,并能促进C -myc、TGF -β1的表达 ,抑制BCL -2表达。Objective The relationship between deficient Se mouse with viral myocarditis and apoptosis had been studied in this paper.Methods Male BALB/C mice (5-week-old) were randomly divided into I experimental group, Ⅱ control group and were fed Se-deficient and Se-normal food respectively. After 5 weeks, mice in groupⅠ were intraperitoneally injected CVB 3m10 33 TCD 50 by the dosage of 0.1ml as well as mice in groupⅡ with the same dosage 1640 liquor.Results Pathological changes of myocardial issues were observed through LT and ET after mice were killed 7 days later original injection.The results showed that ,by LT, detection rates of pathological change between mice in groupⅠ(75%) and group Ⅱ(35%) are obviously different (χ 2 check P<0.05). By means of TDT/dUTP nick-end labelling method (TUNEL), apoptosis cells and expression of C-myc and TGF-β 1 could been found in myocardium of Se-deficient diet feeding mice and regular diet feeding mice. No or less apoptosis could been observed in the regions where BCL-2 expressed highly.Conclusions Results of this project showed that Se-deficiency could increase apoptosis high expression in myocardial tissues to CVB 3m attack virus. Se-deficiency could increase C-myc 、TGF-β 1 high expression.
分 类 号:R542.21[医药卫生—心血管疾病]
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