中文摘要：

目的 探讨靳三针对宫内窘迫HIBD大鼠大脑皮质Cyt-c和Caspase-3表达的影响,揭示靳三针对大脑的保护机制。方法 SD雌性大鼠妊娠21 d时剖腹,用止血钳夹闭双侧子宫角血管5 min,剖宫产取出幼鼠经行为学及脑组织切片确认缺氧缺血性脑损伤的为模型大鼠,随机分为模型组、针刺组。模型组不针刺;针刺1组、针刺2组、针刺3组、针刺4组分别于出生后第3、5、7、14天开始针刺,连续7 d;正常对照组自然分娩,不造模不针刺。所有组别大鼠均于出生后21 d断头取脑组织,检测大脑皮质中Cyt-c和Caspase-3的表达。结果 4个针刺组的Cyt-c光密度值都有所下降,其中针刺1组、针刺2组与模型组比较差异有统计学意义（P〈0.05）。针刺1组Caspase-3的表达被明显下调,与模型组比较差异有统计学意义（P〈0.05）。结论 出生后第3天开始针刺对宫内窘迫HIBD大鼠脑的保护作用与Cyt-c和Caspase-3表达的下调有关。

英文摘要：

Objective To investigate the effect of jin＇s three-needle scalp electroacupuncture on Cyt-c and Caspase-3 expressions in the cerebral cortex in Intrauterine distress-induced HIBD rats and reveal the mechanism of its protective action on the brain. Method The abdomen was incised in a female SD rat at 21 days of pregnancy. Bilateral uterine horn blood vessels were tightly clamped with a hemostat for five minutes. An infant rat was then taken out by a cesarean section. A rat model of hypoxic-ischemic brain damage was confirmed by the use of a behavior test and brain tissue sections. The rats were randomized into model and acupuncture groups. The model group was not needled. Acupuncture groups 1, 2, 3 and 4 began to be needled at 3, 5, 7 and 14 days after birth, respectively. Acupuncture treatment was given for seven consecutive days. The normal control group was naturally delivered, not used to make a model and not needled. All groups of rats were decapitated to take the brain tissue at 21 days after birth. Cyt-c and Caspase-3 expressions in the cerebral cortex were detected. Result Cyt-c optical density value decreased somewhat in the four acupuncture groups; there was a statistically significant difference between acupuncture group 1 or 2 and the model group（P〈0.05）. Caspase-3 expression was significantly down-regulated in acupuncture group 1; there was a statistically significant difference compared with the model group（P〈0.05）. Conclusion The protective effect of acupuncture beginning at 3 days after birth on the brain is related to the down-regulation of Cyt-c and Caspase-3 expressions in intrauterine distress-induced HIBD rats.