摘要
目的:观察标本配穴电针治疗对慢性心肌缺血模型大鼠凋亡相关蛋白表达及线粒体超微结构的效应及机制。方法:将70只SPF级Wistar雄性大鼠根据随机数字表法分为7组。采用盐酸异丙肾上腺素(ISO)注射制作慢性心肌缺血模型,LY294002组和IGF-1组分别加注LY294002和IGF-1溶液,所有针刺组在造模前进行电针针刺预处理。最后检测凋亡相关蛋白Caspase-3、Caspase-9、Bax、Bcl-2的表达及心肌线粒体超微结构的变化。结果:各组大鼠心肌组织内凋亡相关蛋白表达相比正常组均有不同程度升高(P<0.01),且心肌超微结构有不同程度损伤。与模型组比较,标本配穴组Caspase-3、Caspase-9、Bax均有明显下降(P<0.01),Bcl-2蛋白表达升高(P<0.01)。经电针治疗后,标本配穴组与IGF-1组心肌线粒体损伤程度一致明显改善,且优于内关组。结论:"标本配穴"电针治疗可调节凋亡相关蛋白的表达,减轻心肌线粒体结构损伤,其调节过程及机制有可能通过PI3K/Akt信号通路来实现其保护心肌细胞的腧穴协同作用。
Objective: To observe the effects and explore the mechanism of the combined Biao and Ben acupoints treatment on apoptosis-related protein expression and mitochondrial ultrastructure in rats with chronic myocardial ischemia.Methods: According to the random number table method, 70 normal Wistar male rats were divided into 7 groups. The chronic myocardial ischemia model was made by ISO injection, and the LY294002 group and IGF-1 group were respectively added to give LY294002 solution and IGF-1 solution injection. All acupuncture groups adopt electroacupuncture pretreatment before modeling.Finally, the expressions of apoptosis-related proteins Caspase-3, Caspase-9, Bax and Bcl-2 were tested and the changes of myocardial mitochondrial ultrastructure were observed. Results: The expression of apoptosis-related proteins in myocardial tissue of each group was increased in different degrees compared with the normal group(P<0.01), and the myocardial ultrastructure had different degrees of damage. Compared with the model group, the Caspase-3, Caspase-9 and Bax in the combined Biao and Ben acupoints treatment group were significantly decreased(P<0.01), and the Bcl-2 protein expression was increased(P<0.01).After electroacupuncture treatment, the degree of myocardial mitochondrial damage was significantly improved in the combined Biao and Ben acupoints treatment group and the IGF-1 group, and it was better than the Neiguan(PC6) group. Conclusion: The combined Biao and Ben acupoints treatment can regulate the expression of apoptosis-related proteins and alleviate myocardial mitochondrial structural damage, and the regulation process and mechanism may be through PI3 K/Akt signaling pathway to achieve the synergy of acupoints to protect cardiomyocytes.
作者
望庐山
梁凤霞
李佳
吴松
刘建民
唐宏图
洪亚群
肖凌
王华
WANG Lu-shan;LIANG Feng-xia;LI Jia;WU Song;LIU Jian-min;TANG Hong-tu;HONG Ya-qun;XIAO Ling;WANG Hua(The First College of Clinical Medical Science,China Three Gorges University/Department of Rehabilitation Medicine,Yichang Central People’s Hospital,Yichang 443003,China;College of Acupuncture and Orthopedics,Hubei University of Chinese Medicine/Preventive Treatment by Acupuncture and Moxibustion,Hubei Collaborative Innovation Center,Wuhan 430065,China)
出处
《中华中医药杂志》
CAS
CSCD
北大核心
2019年第3期1160-1165,共6页
China Journal of Traditional Chinese Medicine and Pharmacy
基金
国家自然科学基金面上项目(No.81273865
No.81473789)
国家自然科学基金青年科学基金(No.81403460)
湖北中医药大学校级课题(No.2013-144)~~
关键词
标本配穴
慢性心肌缺血
细胞凋亡
PI3K/Akt信号通路
蛋白表达
线粒体
超微结构
Combined Biao and Ben acupoints
Chronic myocardial ischemia
Apoptosis
PI3K/Akt signaling pathway
Protein expression
Mitochondria
Ultrastructure
