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Title: [Effect of electroacupuncture on expression of hippocampal Caspase-3 in rats with cerebral ischemia/reperfusion injury]. Author: Li ML, Dong MM, Huang CJ, Xu XH, Zhou GP. Journal: Zhen Ci Yan Jiu; 2022 May 25; 47(5):422-7. PubMed ID: 35616416. Abstract: OBJECTIVE: To observe the effect of electroacupuncture (EA) on the expression level of Caspase-3, so as to explore its mechanism in inhibiting apoptosis after cerebral ischemia reperfusion. METHODS: SD male rats were randomly divided into sham-operation, model, EA and Caspase-3 inhibitor groups (n=20 rats in each group). The focal cerebral ischemia/reperfusion injury rat model was established by occlusion of the middle cerebral artery. Rats of the EA group received EA at "Hegu" (LI4), "Chize" (LU5), "Zusanli" (ST36) and "Sanyinjiao" (SP6) on the affected side for 20 min. Rats of the inhibitor group were given intracerebroventricular injection of inhibitor Z-DEVD-FMK 5 μg before modeling. The neurological deficit scores (NDS) were assessed by using Longa's method, the infarct size of the brain assessed after staining with 2% triphenyltetrazolium chloride. The apoptosis index of nerve cells were observed by TUNEL staining, PCR and Western blot were used to detect the mRNA and protein expressions of Caspase-3 in the hippocampus, separately. RESULTS: After modeling, the NDS, infarct volume, the apoptosis index of hippocampus CA1 area, and Caspase-3 mRNA and protein expression levels were significantly increased in the model group compared with the sham-operation group (P<0.01). After intervention, the NDS, infarct volume, the apoptosis index, Caspase-3 mRNA and protein expression levels were all significantly decreased in the EA and Caspase-3 inhibitor groups re-levant to the model group (P<0.05). CONCLUSION: EA can improve the neurological function in cerebral ischemia/reperfusion rats, which may be related to its effect in inhibiting of Caspase-3 expression. 目的:观察电针对脑缺血再灌注损伤大鼠海马半胱氨酸天冬氨酸蛋白酶-3(Caspase-3)表达的影响, 探讨电针抗脑缺血再灌注损伤后细胞凋亡的作用机制。方法:雄性SD大鼠随机分为假手术组、模型组、电针组及抑制剂组, 每组20只。除假手术组外, 其他各组大鼠采用改良的Longa线栓法建立局灶性脑缺血再灌注损伤模型。造模成功后, 电针组大鼠于患侧“合谷”“尺泽”“足三里”“三阴交”给予电针干预1次, 20 min;抑制剂组于造模前30 min经侧脑室注入Caspase-3抑制剂Z-DEVD-FMK。观察各组大鼠神经功能缺损评分的变化, 用TTC染色法观察病灶侧脑梗死情况, TUNEL染色法检测海马CA1区细胞凋亡指数, Western blot法检测海马Caspase-3蛋白表达, 荧光定量PCR法检测海马Caspase-3 mRNA表达。结果:与假手术组比较, 模型组大鼠神经功能缺损评分、脑梗死体积百分比、海马CA1区细胞凋亡指数、海马Caspase-3蛋白及mRNA表达水平均明显升高(P<0.01)。与模型组比较, 电针组、抑制剂组的神经功能缺损评分、脑梗死体积百分比、海马CA1区细胞凋亡指数、海马Caspase-3蛋白及mRNA表达水平均下降(P<0.05)。结论:电针能对脑缺血再灌注损伤产生保护作用, 其调控机制之一可能是电针刺激通过抑制Caspase-3表达, 发挥其抗细胞凋亡作用, 进而达到其抗脑缺血再灌注损伤的作用。.[Abstract] [Full Text] [Related] [New Search]