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作 者:陆化梅 于国军 郭永娟 耿智隆[2] Lu Huamei;Yu Guojun;Guo Yongjuan;Geng Zhilong(Department of Anesthesiology,Luoyang Orthopedic-traumatological Hospital(Henan Orthopedic Hospital),Henan province,Luoyang 471000;Department of Anesthesiology,940 Hospital of the Joint Logistic Support Unit of the People's Liberation Army of China(formerly Lanzhou Military Region General Hospital),Lanzhou 730000)
机构地区:[1]河南省洛阳正骨医院(河南省骨科医院)麻醉科,洛阳471000 [2]解放军联勤保障部队第940医院麻醉科(原兰州军区总医院),兰州730000
出 处:《数理医药学杂志》2021年第1期7-9,共3页Journal of Mathematical Medicine
基 金:全军面上项目(CLZ1L0)。
摘 要:目的:探讨电针足三里对于重度失血性休克大鼠肝损伤的影响及可能的机制。方法:取60只SD大鼠随机分为对照组(C组)、休克组(S组、SEN组)、复苏组(LR组、LREN1组、LREN2组),采用改良wigger's法复制重度失血性休克模型,检测各组大鼠血浆AST、ALT含量,肝组织TNF-α和MIP-2蛋白表达,MPO活性,电镜下观察肝组织病理学变化。结果:与休克组比较,各复苏组血浆AST、ALT含量,肝组织TNF-α和MIP-2蛋白表达增加,MPO活性降低,肝组织超微结构受损明显;与LR组比较,LREN1组及LREN2组以上损伤减轻,其中LREN2组以上指标降低显著(P<0.05),肝组织病理损伤较轻。结论:休克期电针刺激双侧足三里能减轻重度失血性休克再灌注后肝脏损伤,其机制与降低肝组织TNF-α、MIP-2产生,降低MPO活性有关。Objective:To explore the effect and possible mechanism of electroacupuncture on liver injury in rats with severe hemorrhagic shock.Methods:60 SD rats were randomly divided into control group(group C),shock group(group S,group SEN),and resuscitation group(group LR,group LREN1,group LREN2).The hemorrhagic shock model was made through improved Wigger’s method.The contents of plasma AST and ALT,the expression of TNF-αand MIP-2 protein in liver tissues,MPO activity were detected,and the pathological changes of liver tissues were observed under electron microscope.Results:Compared with shock group,the contents of plasma AST and ALT,expressions of TNF-αand MIP-2 protein in liver significantly increased,while MPO activity decreased and the ultrastructure of liver tissue was damaged obviously in resuscitation group.The injury in LREN1 group and LREN2 group was alleviated compared with that in LR group,the above indexes decreased significantly in the LREN2 group(P<0.05),and the pathological injury of liver tissue was mild.Conclusion:Electroacupuncture stimulation of bilateral Zusanli during shock can reduce liver injury after reperfusion of severe hemorrhagic shock.The mechanism is related to reducing TNF-α,MIP-2 production of liver tissue and MPO activity.
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