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机构地区:[1]辽宁中医药大学针灸推拿学院,辽宁110032
出 处:《北京中医药大学学报》2016年第2期173-176,共4页Journal of Beijing University of Traditional Chinese Medicine
基 金:国家重点基础研究发展计划(973计划)项目(No.2012CB518503);高等学校博士学科点专项科研基金(No.20122133120001)
摘 要:目的观察循经针刺对异丙肾上腺激素诱导的心肌缺血大鼠心肌组织Toll样受体4(TLR4)蛋白表达的影响。方法将50只雄性SD大鼠随机分成正常组、模型组、内关组、列缺组、非经非穴组(每组10只),除正常组外其余4组均采用皮下注射异丙肾上腺激素建立大鼠心肌缺血模型。造模成功后,内关组、列缺组、非经非穴组分别电针大鼠双侧内关穴、列缺穴以及非经非穴(神阙穴与天枢穴连线中点),每天1次,共7 d。末次治疗后取材,观察各组大鼠心脏组织病理切片、血清超氧化物歧化酶(SOD)、心肌组织肌酸激酶同工酶(CK-MB)含量和TLR4蛋白表达水平。结果与模型组比较,内关组心肌纤维排列整齐、结构完整、细胞间质炎细胞浸润不明显,血清SOD水平明显升高(P<0.01),心肌组织中CK-MB含量明显降低(P<0.01)、TLR4蛋白表达显著减弱(P<0.01)。而列缺组、非经非穴组与模型组之间比较以上各指标均无明显差别(P>0.05)。结论循经电针内关穴可对心肌缺血大鼠产生治疗作用,其机制之一可能是通过调节心肌组织TLR4蛋白表达而实现的。Objective To study the effects of electro acupuncture( EA) on selected acupoints along meridians on cardiac Toll-like receptor 4( TLR4) in SD rats with myocardial ischemia induced by isoprenaline hydrochloride( ISO). Methods 50 male SD rats were randomly divided into five groups( n = 10each). ISO was subcutaneously injected in all groups except the blank group to establish the myocardial ischemia model. After successful modeling,EA was applied at corresponding acupuncture point for rats in the Neiguan( PC6) group,the Lieque( LU7) group and the non-acupoint( mid-point between RN8 and ST25) group. Myocardial tissue of the rats were obtained after the final EA. Superoxide dismutase( SOD) activities,creative kinase( CK-MB),morphology of cardiac tissue and cardiac TLR4 protein expression were evaluated. Results Compared with the model group,the rats of PC6 group myocardial fibers were arranged more and appeared more orderly with complete structure; cell interstitial infiltration of inflammatory cells was not apparent. The serum SOD contents were significantly increased,while the levels of CK-MB and TLR4 protein in myocardial tissue were significantly decreased. There were no significant differences between the above parameters in the non acupoint group and the LU7 group when compared to model group. Conclusion The mechanism of the therapeutic effect of EA at Neiguan( PC6) on myocardial ischemia is probably by regulating the expression of myocardial tissue TLR4 protein.
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