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电针对血管性痴呆大鼠脑组织中脑源性神经营养因子、脂肪酸结合蛋白、脂蛋白相关磷脂酶A2的影响 被引量:5

Effect of Acupuncture on BDNF,H-FABP,Lp-PLA2 in Brain Tissue of Vascular Dementia Rats
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摘要 目的研究电针对血管性痴呆(vascular dementia,VD)大鼠脑组织中脑源性神经营养因子(brain-derived neurotrophic factor,BDNF)、脂肪酸结合蛋白(heart type-fatty acid binding protein,H-FABP)和脂蛋白相关磷脂酶A2(Lipoprotein-associated phospholipase A2,Lp-PLA2)的影响,探讨针灸治疗VD的作用机制。方法将40只健康SD大鼠,按随机数字表法分为正常组和针灸组、药物组、对照组,每组10只。除正常组外,其余3组通过反复夹闭双侧颈总动脉再注射硝普钠的方法制成VD大鼠。正常组与对照组不作任何治疗。药物组以尼莫地平+蒸馏水调制成悬浊液标准,按体重300 mg/kg灌胃治疗。针灸组选取“百会”“水沟”“太冲”“合谷”“足三里”,常规消毒后采用电针针刺治疗。各组均进行学习和记忆的行为学测试,最后全部断头处死,检测大鼠脑组织中BDNF、H-FABP和Lp-PLA2含量。结果4组大鼠学习记忆能力强弱的顺序依次为正常组>针灸组>药物组>对照组,各组间比较,差异均有统计学意义(P<0.05,P<0.01)。对照组与正常组比较,脑组织中的BDNF含量明显降低,Lp-PLA2和H-FABP含量降低更明显,差异有统计学意义(P<0.05,P<0.01)。药物组与对照组比较,脑组织中BDNF和Lp-PLA2含量明显提升,H-FABP含量则提升幅度更明显,差异有统计学意义(P<0.05,P<0.01)。针灸组与药物组比较,脑组织中BDNF含量较明显提升,而Lp-PLA2和H-FABP含量则提升幅度更大,差异有统计学意义(P<0.05,P<0.01)。结论脑组织中BDNF、H-FABP和Lp-PLA2含量能反映其神经功能,穴位电针治疗能修复VD大鼠神经元,促进脑组织中BDNF、H-FABP和Lp-PLA2的高表达,改善认知功能。 Objective To study the effects of acupuncture on brain-derived neurotrophic factor(BDNF),fatty acid binding protein(H-FABP)and lipoprotein-related phospholipase A2(Lp-PLA2)in the brain tissue of vascular dementia(VD)rats,and to explore the mechanism of acupuncture and moxibustion in controlling VD.Method 40 healthy SD rats were divided into normal group and group according to random number table.Acupuncture group,drug group,control group,10 rats in each group.Except for the normal group,the other 3 groups were made into VD rats by repeatedly clamping the bilateral common carotid arteries and then injecting sodium nitroprusside.The normal group and the control group did not receive any treatment.The drug group was treated with nimodipine+distilled water to prepare a suspension standard,and the body weight was 300 mg/kg gavage treatment.The acupuncture group was treated at“Baihui”,“Shuigou”,“Taichong”,“Hegu”,and“Zusanli”acupoints.After routine disinfection,electroacupuncture was used for treatment.Each group was subjected to behavioral tests of learning and memory.Finally all rats were killed by decapitation,andthe contents of BDNF,H-FABP and Lp-PLA2 in the brain tissue of rats were detected.Results In the 4 groups of experimental rats,the order of learning and memory ability was normal group>acupuncture treatment group>medicine treatment group>control group,and the differences between the groups are statistically significant(P<0.05,P<0.01).Comparison between the control group and the normal group,the content of BDNF in the brain tissue of control group was significantly lower than that in normal group,and the content of Lp-PLA2 and H-FABP was lower,and the difference was statistically significant(P<0.05,P<0.01).Compared with the control group,BDNF and Lp-PLA2 in the brain tissue in drug treatment group content increased significantly;H-FABP content increased even more,the difference was statistically significant(P<0.05,P<0.01).Compared with the drug group,the content of BDNF in brain tissue of was significantly increased in the acupuncture group,while the content of Lp-PLA2 and H-FABP increased obviously,and the difference was statistically significant(P<0.05,P<0.01).Conclusion The content of BDNF,HFABP and Lp-PLA2 in brain tissue can reflect its neurological function.Acupuncture treatment can repair VD rat neurons,promote the high expression of BDNF,HFABP and Lp-PLA2 in brain tissue,and improve cognition function.And curative effect is significantly better than drug treatment.
作者 李娜 孙嫘 郭新荣 王卫刚 LI Na;SUN Lei;GUO Xin-rong;WANG Wei-gang(School of Acupuncture and Tuina,Shaanxi University of Traditional Chinese Medicine,Xianyang Shaanxi 712046;Department of Acupuncture and Tuina,Affiliated Hospital of Shaanxi University of Traditional Chinese Medicine,Xianyang Shaanxi 712046)
出处 《世界中西医结合杂志》 2021年第8期1453-1456,1463,共5页 World Journal of Integrated Traditional and Western Medicine
基金 陕西省自然科学基础研究项目(2020JQ-860)。
关键词 血管性痴呆 针灸疗法 脑源性神经营养因子 脂肪酸结合蛋白 脂蛋白相关磷脂酶A2 Vascular Dementia Acupuncture Therapy Brain-Derived Neurotrophic Factor Fatty Acid Binding Protein Lipoprotein-Related Phospholipase A2
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