Weilan Qin, Yan Yan, Xuemei Liu, Wei Shen, Xiaohan Liu, Qingke Ma, Ying Wang, Xianglan Jin
Acupuncture and Moxibustion Department, Dongfang Hospital, Beijing University of Chinese Medicine,100078, Beijing, China.
Center Laboratory, Dongfang Hospital, Beijing University of Chinese Medicine,100078, Beijing, China.
Cell Mol Biol (Noisy-le-grand). 2018 Oct 30;64(13):107-112.
To investigate the effect of medicated thread moxibustion onapoptosis in hippocampal neuronsin a rat model of chronic cerebral ischemic vascular dementia. A total of 40 male Wistar rats were randomly divided into normal group and sham-operated group (7 rats each), and rat model of chronic cerebral ischemic vascular dementia (14 rats). The model group rats were treated with medicated thread moxibustion two weeks after surgery, once a day, with one day break every six days, (24 times in all)and an observation period of 4 weeks. At the end of therapy, H&E staining was used to monitor changes in the neurons in CA1 area of the rat hippocampus. Changes in related indexes such as Bax, Bc1-2 and C-fos of neuron apoptosis in hippocampus CA1 area were determined by immunohistochemistry, while protein expression was semi-quantitatively assayed using imaging analysis technique. There was significant hippocampal neuronal necrosis six weeks after model establishment, but the necrosis was milder in rats in the medicated thread moxibustion group. Bax and C-fos were positively expressed and significantly higher in the hippocampus of chronic cerebral ischemic vascular dementia rats (model group) than in the medicated thread moxibustion group after treatment (p <0.01). The expression of Bcl-2 was increased in the medicated thread group after treatment, and was higher in the model group, but comparable to that in the sham-operated group (p=0.975>0.05). Medicated thread moxibustion alleviates hippocampal neuronal necrosis, inhibits neuron apoptosis in hippocampus CA1 area, protects nerves, and maintains relative equilibrium inBax/Bcl-2 through down-regulation of C-fos and Bax and up-regulation of Bcl-2. Thus, cell apoptosis-related pathway may be one of its mechanisms of action.
探讨药线灸对慢性脑缺血性血管性痴呆大鼠模型海马神经元凋亡的影响。将40只雄性Wistar大鼠随机分为正常组和假手术组(每组7只),以及慢性脑缺血性血管性痴呆大鼠模型组(14只)。模型组大鼠术后两周采用药线灸治疗,每日1次,每6日休息1天,共治疗24次,观察期为4周。治疗结束时,采用苏木精-伊红(H&E)染色观察大鼠海马CA1区神经元的变化。采用免疫组织化学法检测海马CA1区神经元凋亡相关指标Bax、Bcl-2和C-fos的变化,同时采用图像分析技术对蛋白表达进行半定量分析。造模6周后海马神经元出现明显坏死,但药线灸组大鼠坏死程度较轻。慢性脑缺血性血管性痴呆大鼠(模型组)海马中Bax和C-fos呈阳性表达,且明显高于治疗后的药线灸组(p<0.01)。治疗后药线灸组Bcl-2表达升高,模型组高于药线灸组,但与假手术组相当(p = 0.975>0.05)。药线灸可减轻海马神经元坏死,抑制海马CA1区神经元凋亡,保护神经,并通过下调C-fos和Bax、上调Bcl-2维持Bax/Bcl-2的相对平衡。因此,细胞凋亡相关途径可能是其作用机制之一。