电针对局灶性脑缺血大鼠缺血区脑组织神经细胞凋亡及神经生长因子影响的研究

目的 :观察电针督脉经穴“大椎”、“百会”对大鼠缺血区脑组织神经细胞凋亡及NGLF的影响。方法 :用凝闭一侧大脑中动脉的脑缺血大鼠为动物模型 ,采用TUNEL染色法和免疫组化染色S P法进行观察。结果 :缺血 +电针组中 ,大脑皮层梗塞区内TUNEL染色阳性细胞较缺血组显著减少 (P <0 0 1 ) ,NGFR免疫阳性表达在细胞数量上及强度上也均较缺血组及假手术组明显增强 (P <0 0 1 )。结论 :电针能抑制脑缺血后脑内神经细胞的凋亡 ,可增强局灶性脑缺血大鼠脑组织的NGFR的表达 ,对缺血性脑损伤具有一定的保护作用。为临床针灸治疗缺血性脑血管疾病奠定了理论基础

Study on the Effect of Electroacupuncture on Apoptosis and Nerve Growth Factor of Cerebral Tissues in Rats with Focal Brain Ischemia

Objective: To observe the effect of electroacupuncture (EA) of "Dazhui"(GV 14) and "Baihui"(GV 20) on apoptosis and nerve growth factor (NGF) expression in rats with cerebral ischemia. Methods: 24 Wistar rats were randomly and evenly divided into sham-operation group, ischemia group and EA+ischemia group. Local brain ischemia was produced by occlusion of the middle cerebral artery (MCAo). "Dazhui"(GV 14) and "Baihui"(GV 20) were punctured with filiform needles and stimulated electrically with an EA therapeutic apparatus (5～10 Hz, dense-sparse waves, 3～5 V and stimulating duration of 30 min). The rat's cerebral tissues of various groups were cut into sections to be stained with immunohistochemical method. The TUNEL method was used to display apoptosis state and S-P method employed to show NGF expression. Results: TUNEL staining showed that the number of the died neurocytes in sham-operation group, ischemia group and ischemia+EA group were 0, 676±12 and 326±15 respectively, suggesting that EA could evidently suppress apoptosis of the ischemic cerebral tissues. S-P staining method showed that the number of NGF receptor immunoreaction positive cells of sham-operation group, ischemia group and ischemia+EA group were 2.0±0.3, 6.0±0.3 and 35.0±2.0 separately. In addition, the density of the immunoreaction positive cell staining was also higher in EA+ischemia group. It suggested that EA could remarkably potentiate NGFR expression in the ischemic cerebral tissues (P<0.01). Conclusion: EA can relieve apoptosis of the ischemic cerebral tissues and strengthen NGF expression, suggesting that EA has a certain protective action on ischemic cerebral injury through up-regulation of the expression of NGF.