兰州大学机构库 >学院待认领
抑制炎性反应双通路对心肌缺血再灌注损伤预后的影响及机制研究
Alternative TitleThe prognosis effect and mechanics research of myocardial ischemia-reperfusion injury based on inhibit inflammatory response double pathways
李沛鸿
Thesis Advisor张卫泽
2013-05-14
Degree Grantor兰州大学
Place of Conferral兰州
Degree Name硕士
Keyword腺病毒 可溶性补体I型受体 可溶性肿瘤坏死因子受体I 心肌缺血 再灌注损伤
Abstract目的:针对心肌缺血再灌注损伤发生的补体活化途径和炎性细胞因子反应瀑布途径,采用联合使用重组腺病毒介导的可溶性补体I型受体(sCR1)及可溶性肿瘤坏死因子受体I(sTNFR1)于再灌注前预处理,探讨其联合应用对拮抗心肌缺血再灌注炎性损伤的协同效果及其机制。方法:实验一:30只SD雌性SPF级大鼠,250±50g,随机等分为3组( n= 10):( 1)假手术对照组:仅开胸不结扎;(2)缺血/再灌注(I/R)模型组(Ad-LacZ);(3) Ad-sCR1/sTNFRI联合组。预处理造模完毕后2W做血液及心肌组织相关检测。实验二:50只SD雌性SPF级大鼠,250±50g,随机等分为5组(n=10):(1)假手术对照组:仅开胸不结扎;(2)缺血/再灌注(I/R)模型组(Ad-LacZ);(3)Ad-sCR1干预组;(4)Ad-sTNFRI干预组;(5)Ad-sCR1/sTNFRI联合组。预处理造模完毕后2W做血液及心肌组织相关检测。结果表明Ad-sCR1/sTNFRI组使Cx43表达、分布和改善明显优于模型组且接近于正常组。Ad-sCR1和Ad-sTNFRI都能使心肌缺血再灌注损伤大鼠血清中LDH、MDA含量降低,SOD的活力升高;大鼠心肌组织病理学切片镜下所见,Ad-sCR1和Ad-ssTNFRI干预组大鼠心肌组织病变程度较轻;预处理后的每组都上调血浆及组织水平的可溶性TNFR表达,抑制了炎性因子TNF-的表达,且Ad-sCR1/sTNFRI组结果较 Ad-sCR1和Ad-sTNFRI组都显著,都具有显著性差异。
Other AbstractObjective The joint use of recombinant adenovirus-mediated sCR1 and sTNFR1 of reperfusion pretreatment, explore synergy against myocardial ischemia-reperfusion injury and its mechanism of joint application.Methods All female SD rats, randomly divided into five groups (n=10):(Sham-operated groups; Ischemia/reperfusion model group;Ad-Scr1 groups;Ad-sTNFR1 group;Ad-sCR1/s TNFRI group. Pretreatment modeling is completed after 2 weeks to do the detection of blood and myocardial tissue.Results Ad-sCR1/sTNFR1 enable Cx43 expression, distribution and improved significantly better than the model group and close to the normal group; Ad-sCR1 and Ad-sTNFR1 can myocardial ischemia-reperfusion injury in rat serum of LDH, CK and MDA decreased significantly, SOD in significantly higher; The Ad-sCR1 and the Ad-sTNFR1 group rat myocardial tissue lesions to a lesser extent; Each raised pretreated plasma and tissue levels of sTNFR1 expression, Inhibited the expression of TNF-, The Ad-sCR1/sTNFR1 set of results than Ad-SCR1 and the Ad-sTNFR1 group were significantly ( P < 0. 01).
URL查看原文
Language中文
Document Type学位论文
Identifierhttps://ir.lzu.edu.cn/handle/262010/222337
Collection学院待认领
Affiliation临床医学院
Recommended Citation
GB/T 7714
李沛鸿. 抑制炎性反应双通路对心肌缺血再灌注损伤预后的影响及机制研究[D]. 兰州. 兰州大学,2013.
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