Liu Yang, Zhang Jie, Zan Jingwei, Zhang Fengxian, Liu Guokai, Wu Anshi
Department of Anesthesiology, Beijing Chao-Yang Hospital, Capital Medical University, Beijing 100020, P.R. China.
Department of Anesthesiology, Dongzhimen Hospital, Beijing University of Chinese Medicine, Beijing 100700, P.R. China.
Exp Ther Med. 2020 Jul;20(1):495-499. doi: 10.3892/etm.2020.8688. Epub 2020 Apr 27.
Influence of lidocaine on rats with cerebral ischemia-reperfusion injury (CIRI) was studied to explore its mechanism of action. A total of 30 Sprague-Dawley rats were randomly divided into control group and model group, and the rat model of CIRI was prepared by the suture-occluded method in the model group. Then the rats in the model group were randomly assigned into the model group (n=10) and the lidocaine group (n=10). The neurological function score of rats was evaluated, and the levels of serum B-cell lymphoma-2 (Bcl-2) and Bcl-2 associated X protein (Bax) in rats were determined using ELISA. TUNEL assay was performed to detect the neuronal apoptosis in the brain of rats. The messenger ribonucleic acid (mRNA) and protein expression levels of cyclic adenosine monophosphate (cAMP) and protein kinase A (PKA) were measured via RT-PCR and western blotting, respectively. Compared with those in the control group, the rats in the model group had an elevated neurological function score, a raised level of Bcl-2, but a reduced level of Bax in the serum, an obviously increased rate of neuronal apoptosis in the brain and decreased mRNA and protein levels of cAMP and PKA in cerebral tissues. The rats in lidocaine group had a lower neurological function score, a lower level of Bcl-2, but a higher level of Bax in the serum, an evidently lower rate of neuronal apoptosis in the brain and higher mRNA and protein levels of cAMP and PKA in cerebral tissues than those in the model group. Lidocaine can improve the neurological function of rats with CIRI and inhibit neuronal apoptosis in the brain, and its mechanism of action may be related to the activation of the cAMP/PKA signaling pathway.
研究利多卡因对脑缺血再灌注损伤（CIRI）大鼠的影响，以探讨其作用机制。将30只Sprague-Dawley大鼠随机分为对照组和模型组，模型组采用线栓法制备CIRI大鼠模型。然后将模型组大鼠随机分为模型组（n = 10）和利多卡因组（n = 10）。评估大鼠的神经功能评分，采用ELISA法测定大鼠血清中B细胞淋巴瘤-2（Bcl-2）和Bcl-2相关X蛋白（Bax）的水平。采用TUNEL法检测大鼠脑内神经元凋亡情况。分别通过RT-PCR和western blotting检测环磷酸腺苷（cAMP）和蛋白激酶A（PKA）的信使核糖核酸（mRNA）和蛋白表达水平。与对照组相比，模型组大鼠神经功能评分升高，血清中Bcl-2水平升高，但Bax水平降低，脑内神经元凋亡率明显增加，脑组织中cAMP和PKA的mRNA和蛋白水平降低。利多卡因组大鼠神经功能评分低于模型组，血清中Bcl-2水平降低，但Bax水平升高，脑内神经元凋亡率明显降低，脑组织中cAMP和PKA的mRNA和蛋白水平高于模型组。利多卡因可改善CIRI大鼠的神经功能，抑制脑内神经元凋亡，其作用机制可能与激活cAMP/PKA信号通路有关。
