利多卡因对肾缺血再灌注大鼠心肌组织C-Jun氨基末端激酶和细胞外调节蛋白激酶表达的影响

发布时间：2018-06-07 15:54

本文选题：再灌注损伤 + 利多卡因　；参考：《中国老年学杂志》2017年11期

【摘要】：目的评价利多卡因预先给药对肾缺血再灌注(I/R)大鼠心肌组织C-Jun氨基末端激酶(JNK)和细胞外调节蛋白激酶(ERK)表达的影响。方法健康Wistar大鼠36只,体重300~350 g,采用随机数字表法分为3组(n=12):假手术组(S组)只分离肾动脉不夹闭;I/R组,双肾缺血60 min、恢复灌注4 h建立大鼠I/R损伤模型;利多卡因预先给药组(L组)夹闭双侧肾动脉前60 min时前静脉注射利多卡因5 mg/kg,随后以2 mg·kg~(-1)·h~(-1)速率静脉输注60 min;S组和I/R组给予等容量生理盐水。再灌注4 h时取心脏血样,采用酶联免疫吸附法(ELISA)法测定心肌肌钙蛋白I(cTnI)浓度,随后处死大鼠,取心肌组织,测定心肌丙二醛(MDA)含量和超氧化物歧化酶(SOD)活性,采用Western法测定心肌细胞JNK和ERK的表达水平,光镜下观察心肌组织及肾组织病理学改变。结果光镜下可见I/R组呈明显心肌及肾组织损伤的形态学变化,L组心肌组织及肾组织损伤明显减轻。与S组比较,I/R组心肌组织JNK及ERK表达水平升高,血清cTnI浓度、心肌MDA含量升高,SOD活性降低(P0.05);与I/R组比较,L组心肌组织JNK表达水平降低,ERK表达水平升高,血清cTnI浓度、心肌MDA含量降低,SOD活性升高(P0.05)。结论利多卡因预先给药可减轻I/R大鼠心肌损伤,其机制可能与激活MAPK信号传导通路,上调ERK和下调JNK表达有关。
[Abstract]:Objective to evaluate the effects of lidocaine on the expression of C-Jun amino-terminal kinase (C-Jun) and extracellular regulated protein kinase (ERK) in myocardial tissue of rats with renal ischemia reperfusion (I / R). Methods Thirty-six healthy Wistar rats, weighing 300,350g, were randomly divided into 3 groups: sham operation group (S group): I / R group with no clamping of renal artery. I / R injury model of rats was established after 60 min of ischemia and 4 h of reperfusion. Lidocaine group (n = 60) was injected with lidocaine 5 mg / kg at 60 min before occlusion, and then was given isovolumic saline at a rate of 2 mg / kg ~ (-1) h ~ (-1) / h ~ (-1) (n = 60 min) and I / R group (n = 60). Cardiac blood samples were taken at 4 h after reperfusion. Cardiac troponin I cTnI concentration was measured by Elisa. Then the rats were killed, myocardial tissue was taken, the content of malondialdehyde (MDA) MDAs and the activity of superoxide dismutase (SOD) were measured. The expression of JNK and ERK in cardiac myocytes was measured by Western method. The pathological changes of myocardial and renal tissues were observed under light microscope. Results under light microscope, I / R group showed obvious morphologic changes of myocardial and renal tissue injury. Compared with group S, the expression of JNK and ERK in myocardial tissue of group I / R increased, the concentration of cTnI in serum and the content of MDA in myocardium increased and the activity of MDA decreased (P 0.05), and the expression of JNK in myocardium of group I / R decreased the expression of JNK and the concentration of cTnI in serum. The content of MDA in myocardium decreased and the activity of sod increased (P 0.05). Conclusion Lidocaine can attenuate myocardial injury in I / R rats, and its mechanism may be related to activation of MAPK signaling pathway, up-regulation of ERK and down-regulation of JNK expression.
【作者单位】：中山市中医院麻醉科;
【分类号】：R965

【相似文献】