首页|利多卡因调节RhoA/ROCK信号通路对缺血性脑卒中大鼠的神经保护作用

利多卡因调节RhoA/ROCK信号通路对缺血性脑卒中大鼠的神经保护作用

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目的 探讨利多卡因调节RhoA/ROCK信号通路对缺血性脑卒中(IS)大鼠神经保护作用.方法 通过线栓法建立模型IS大鼠,随机分为模型组、利多卡因低(利多卡因-L,5mg/kg)、中(利多卡因-M,10 mg/kg)、高剂量(利多卡因-H,20mg/kg)组以及利多卡因-H+溶血磷脂酸(LPA)(20 mg/kg利多卡因+50μmoL/LLPA)组,以仅分离但不插尼龙线的大鼠为假手术组;干预结束后,对大鼠进行神经功能评分、脑梗死体积、脑含水量测定;分离脑组织,观察神经元变化、神经细胞凋亡以及RhoA、ROCK蛋白表达.结果 与假手术组相比,模型组大鼠Zea-Longa评分(3.28±0.33、0.14±0.02)、脑梗死体积(38.09±3.81、0.00±0.00)、含水量(84.11±2.39、62.95±0.65)、神经细胞凋亡率(39.51±3.96、5.14±0.52)、RhoA(1.16±0.12、0.24±0.03)、ROCK蛋白(2.15±0.22、0.77±0.08)表达增加(P<0.05);与模型组相比,利多卡因组大鼠Zea-Longa评分(2.37±0.24、1.52±0.16、0.87±0.09)、脑梗死体积(27.42±2.76、16.64±1.68、8.22±0.83)、含水量(75.24±1.46、68.34±1.02、63.15±0.86)、神经细胞凋亡率(27.08±2.71、18.84±1.89、9.47±0.95)、RhoA(0.78±0.08、0.52±0.06、0.26±0.03)、ROCK蛋白(1.66±0.17、1.24±0.13、0.86±0.09)表达显著降低,组间差异有统计学意义(P<0.05);LPA逆转了利多卡因-H对IS大鼠的保护作用.结论 利多卡因通过抑制RhoA/ROCK信号通路对IS大鼠发挥神经保护作用.
Neuroprotective effect of lidocaine on ischemic stroke rats by regulating the RhoA/ROCK signaling pathway
Objective To investigate the neuroprotective effect of lidocaine on ischemic stroke(IS)rats by regulating the RhoA/ROCK signaling pathway.Methods A model of IS rats was established by thread occlusion method and randomly separated into model group,lidocaine low(lidocaine-L,5 mg/kg),medium(lidocaine-M,10 mg/kg),high-dose(lidocaine-H,20 mg/kg)groups,and lidocaine-H+Lysophosphatidic acid(LPA)(20 mg/kg li-docaine+50 μmoUL LPA)group,rats that were separated but not inserted with nylon thread were in the sham opera-tion group,after the intervention,the neurological function score,cerebral infarction volume,and brain water con-tent of the rats were measured;brain tissue was isolated,and changes in neurons,neuronal apoptosis,and expres-sion of RhoA and ROCK proteins were observed.Results Compared to the sham group,Zea-Longa score(3.28±0.33,0.14±0.02),cerebral infarction volume(38.09±3.81,0.00±0.00),water content(84.11±2.39,62.95±0.65),apoptosis rate(39.51±3.96,5.14±0.5)in model group 2),RhoA(1.16±0.12,0.24±0.03),ROCK protein(2.15±0.22,0.77±0.08)were increased(P<0.05);Compared to the model group,Zea-Longa score(2.37±0.24,1.52±0.16,0.87±0.09),cerebral infarction volume(27.42±2.76,16.64±1.68,8.22±0.83),water content(75.24±1.46,68.34±1.02,63.15)in lidocaine group±0.86),neuronal apoptosis rate(27.08±2.71,18.84±1.89,9.47±0.95),RhoA(0.78±0.08,0.52±0.06,0.26±0.03),ROCK protein(1.66±0.17,1.24±0.13,0.86±0.09)The expression was significantly decreased and there were differences between groups(P<0.05);LPA reversed the protective effect of li-docaine-H on IS rats.Conclusion Lidocaine exerts neuroprotective effects on IS rats by inhibiting the RhoA/ROCK signaling pathway.

lidocaineIschemic strokeRhoA/ROCKNeuroprotectionAnimal model

丁迪卿、李菁、彭生、杨路宗

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上海中医药大学附属龙华医院麻醉科,上海 200032

利多卡因 缺血性脑卒中 Ras基因同源物A/Rho激酶 神经保护 动物模型

上海市卫生健康委员会科研项目

202240159

2024

解剖学研究
广东省解剖学会 中国解剖学会

解剖学研究

CSTPCD
影响因子:0.327
ISSN:1671-0770
年,卷(期):2024.46(5)