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针刺对合并脑缺血的高脂血症大鼠血清脂质及脑神经营养因子水平的影响

[Effect of acupuncture on serum lipid and cerebral neurogrowth factor levels in hyperlipemia rats with concurrent cerebral ischemia].

作者信息

Ren Xiu-Jun, Ma Hui-Fang, Wang Xiao-Ning, Hong Yin-Zhu, Shi Yu-Cheng, Tu Ya

机构信息

College of Acu-moxibustion, Beijing University of Chinese Medicine, Beijing 100029, China.

出版信息

Zhen Ci Yan Jiu. 2007 Feb;32(1):24-8.

PMID:17580436
Abstract

OBJECTIVE

To observe the effect of electroacupuncture (EA) on serum lipid and cerebral neurogrowth factor (NGF) in rats with hyperlipemia and cerebral ischemia (CI).

METHODS

A total of 36 SD rats were evenly randomized into control, model, EA-I and EA-II groups with 9 cases in each group. Hyperlipemia plus CI model was established by feeding the rats with high-fat foodstuff (6 weeks) and FeCI3-evoked middle-cerebral-artery (MCA) occlusion method. EA (15 Hz, 1-3 mA) was applied to "Sanyinjiao" (SP 6) and "Fenglong" (ST 40) for 20 min, once daily, continuously for 7 days, additionally,"Baihui" (GV 20) and "Shuigou"(GV 26) were punctured and stimulated with hand, which was conducted first before MCA occlusion for rats of group EA-I and after MCA occlusion for rats of group EA-II separately. Fasting blood samples (2 mL/rat) were taken for detecting serum total cholesterol (TC), triglyceride (TG), low density lipid cholesterol (LDL-C) and high density lipid cholesterol (HDL-C) levels. After decapitation of the rats, cerebral tissues were taken, homogenated for detecting NGF content with ABC-ELISA (enzyme-linked immunosorbent assay) and some other cerebral tissues were cut into sections (6 microm)for observing structural changes of the brain after staining with haematoxylin and cosin (HE) method.

RESULTS

Compared with control group, serum TC, TG and LDL-C contents of model, EA-I and EA-II groups increased significantly on day 42 and 59 after modeling (P < 0.01), and HDL-C content of model, EA-I and EA-II groups decreased markedly on day 42 after modeling (P < 0.01). Compared with model group, TC contents of both EA-I and EA-II groups, and TG and LDL-C of EA-I group decreased significantly on day 59 after establishing the model (P < 0.05, 0.01). No significant differences were found between EA-I and EA-II groups in the 4 indexes of blood lipid (P > 0.05). HE staining showed that in model group, neuronal ischemic injury including cellular swelling, edema and nuclear fragmentation in the striatum and the cortex of parietal lobe, widening of the cellular interspace. vacuolation, irregularity of the kytoplasm and karyolemma, etc in CA3 region of hippocampus was apparent, while the situation in EA groups was lighter. Regarding the changes of NGF, compared with control group, NGF contents of model group and EA-I group were significantly lower (P < 0.01); while compared with model group, NGF content of EA-I was significantly higher (P < 0.01); and that of EA-lI group was markedly lower than that of EA-I group (P < 0.05).

CONCLUSION

EA can lower the levels of serum TC, LDL-C and TG and suppress cerebral ischemia plus hyperlipemia induced decrease of NGF level in the brain, which may contribute to its effect in relieving ischemic cerebral injury.

摘要

目的

观察电针对高脂血症合并脑缺血(CI)大鼠血脂及脑源性神经生长因子(NGF)的影响。

方法

将36只SD大鼠随机分为对照组、模型组、电针I组和电针II组,每组9只。采用高脂饲料喂养(6周)结合FeCI3诱发大脑中动脉(MCA)闭塞法建立高脂血症合并CI模型。电针(15Hz,1 - 3mA)刺激“三阴交”(SP 6)和“丰隆”(ST 40)20分钟,每日1次,连续7天,另外,电针I组在MCA闭塞前、电针II组在MCA闭塞后分别针刺并手法刺激“百会”(GV 20)和“水沟”(GV 26)。采集空腹血样(2mL/只大鼠)检测血清总胆固醇(TC)、甘油三酯(TG)、低密度脂蛋白胆固醇(LDL - C)和高密度脂蛋白胆固醇(HDL - C)水平。大鼠断头后,取脑组织匀浆,采用ABC - ELISA(酶联免疫吸附测定)法检测NGF含量,另取部分脑组织切成6微米切片,用苏木精 - 伊红(HE)染色法观察脑组织结构变化。

结果

与对照组相比,模型组、电针I组和电针II组在造模后第42天和59天血清TC、TG和LDL - C含量显著升高(P < 0.01),造模后第42天模型组、电针I组和电针II组HDL - C含量显著降低(P < 0.01)。与模型组相比,造模后第59天电针I组和电针II组的TC含量以及电针I组的TG和LDL - C含量显著降低(P < 0.05,0.01)。电针I组和电针II组血脂4项指标比较差异无统计学意义(P > 0.05)。HE染色显示,模型组纹状体及顶叶皮质神经元缺血性损伤明显,包括细胞肿胀、水肿、核碎裂,海马CA3区细胞间隙增宽、空泡形成、细胞质和细胞核膜不规则等,而电针组情况较轻。关于NGF的变化,与对照组相比,模型组和电针I组NGF含量显著降低(P < 0.01);与模型组相比,电针I组NGF含量显著升高(P < 0.01);电针II组NGF含量明显低于电针I组(P < 0.05)。

结论

电针可降低血清TC、LDL - C和TG水平,抑制高脂血症合并脑缺血诱导的脑内NGF水平降低,这可能是其减轻缺血性脑损伤的作用机制。

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