摘要
探讨川芎嗪(Tetramethylpyrazine,TMP)对实验性自身免疫性脑脊髓炎(experimental autoimmune encephalomyelitis,EAE)小鼠神经元凋亡的调节作用及其机制。40只C57BL/6小鼠注射MOG-35-55制剂建立EAE模型,随机分为PBS组和TMP组,PBS及TMP每日腹腔注射连续给药28 d,取腰椎段脊髓,行免疫荧光染色检测神经元数目。将PC12细胞按照处理不同,分为空白对照组、interferon-γ(IFN-γ)处理组、IFN-γ+TMP组。各组均行流式细胞术检测神经元凋亡情况,Western blotting检测NF-κB、p-NF-κB表达水平。动物实验结果显示与PBS组相比,TMP能明显增加神经元的数量(P<0.05)。而细胞实验结果显示TMP可有效抑制神经元细胞的凋亡(P<0.05),且明显减少了p-NF-κB的表达(P<0.05)。TMP对EAE小鼠有神经保护作用,其机制可能与抑制神经元的凋亡、抑制NF-κB信号通路有关。
To explore the effects and mechanism of tetramethylpyrazine(TMP)on neuronal apoptosis in experimental autoimmune encephalomyelitis(EAE)mice.A total of 40 C57BL/6 mice were injected with MOG-35-55 and pertussis to establish EAE model.They were randomly divided into PBS group and TMP group.PBS and TMP were injected intraperitoneally for 28 days,and lumbar spinal cords of mice were obtained for immunofluorescence staining.The PC12 cells were divided into blank control group,IFN-γgroup and IFN-γ+TMP group.Flow cytometry was used to detect neuron apoptosis,and western blotting was used to detect the expression of NF-κB and p-NF-κB.In vivo experiment showed that compared with the PBS group,TMP can significantly reduce the neuronal apoptosis(P<0.05).In vitro experiment results showed that TMP can effectively inhibit neuronal apoptosis(P<0.05),and reduce the expression of p-NF-κB(P<0.05).Therefore,TMP has a neuroprotective effect on EAE mice,and its mechanism may be related to the inhibition of neuronal apoptosis and the regulation of NF-κB signaling pathway.
作者
巩丽华
周砚秋
王思远
马辰旭
侯云
Gong Lihua;Zhou Yanqiu;Wang Siyuan;Ma Chenxu;Hou Yun(College of Basic Medicine,Binzhou Medical University,Yantai 264003,China)
出处
《山东化工》
CAS
2020年第23期23-26,共4页
Shandong Chemical Industry
基金
山东省自然科学基金(基金号为ZR2016HP05)。
