Sun Yan, Chen Hai, Lin Yibing
School of Rehabilitation Medicine, He'nan University of Chinese Medicine Zhengzhou, He'nan Province, China.
Department of Children's Rehabilitation, The Third Affiliated Hospital of Zhengzhou University Zhengzhou, He'nan Province, China.
Am J Transl Res. 2021 Apr 15;13(4):2213-2223. eCollection 2021.
To investigate the role of rehabilitation training and TLR4/MyD88 signaling pathway on neuronal apoptosis in mice with cerebral ischemic stroke.
Mice were randomized into six groups, which were normal group (healthy mice, n=20), control group (sham surgery, n=20), model group (middle cerebral artery occlusion (MCAO) model, n=20), training (MCAO model, continuous rehabilitation training for 4 weeks, n=20), TAK-242 group (MCAO model, TL R4 inhibitor TAK-242, n=20), and TAK-242 + Training group (MCAO model, TLR4 inhibitor TAK-242 + rehabilitation training, n=20).
Neurobehavioral assessment was performed, and cerebral infarction area of mice was detected by triphenyl tetrazolium chloride staining. Compared with the normal group, no significant differences in all indicators were found in the control group (all P>0.05), while the other groups had higher neurological function scores, cerebral infarction area, neuronal apoptosis rate, increased expressions of TLR4, MyD88, Bax, NF-κB, TNF-α, Caspase-3, IL-1βA and decreased mRNA and protein expressions of Bcl-2 (all P<0.05).
Rehabilitation training can effectively reduce the apoptosis of hippocampal neurons in mice with ischemic stroke by inhibiting the TLR4/MyD88 signaling pathway.
探讨康复训练及Toll样受体4(TLR4)/髓样分化因子88(MyD88)信号通路在脑缺血性脑卒中小鼠神经元凋亡中的作用。
将小鼠随机分为六组,即正常组(健康小鼠,n = 20)、对照组(假手术,n = 20)、模型组(大脑中动脉闭塞(MCAO)模型,n = 20)、训练组(MCAO模型,连续康复训练4周,n = 20)、TAK - 242组(MCAO模型,TLR4抑制剂TAK - 242,n = 20)和TAK - 242 +训练组(MCAO模型,TLR4抑制剂TAK - 242 +康复训练,n = 20)。
进行神经行为学评估,并用氯化三苯基四氮唑染色检测小鼠脑梗死面积。与正常组相比,对照组各项指标差异均无统计学意义(均P>0.05),而其他组神经功能评分、脑梗死面积、神经元凋亡率均较高,TLR4、MyD88、Bax、核因子κB(NF - κB)、肿瘤坏死因子α(TNF - α)、半胱天冬酶3(Caspase - 3)、白细胞介素1β(IL - 1β)表达增加,Bcl - 2的mRNA和蛋白表达降低(均P<0.05)。
康复训练可通过抑制TLR4/MyD88信号通路有效减少缺血性脑卒中小鼠海马神经元凋亡。