井穴刺络放血法对MCAO模型大鼠大脑皮层HSP70蛋白表达的影响

Effect of Collateral Puncture-bloodletting at JING Point on Expression of HSP70 Protein of Cerebral Cortex in Rats with Middle Cerebral Artery Occlusion

[目的]从脑内应激热休克蛋白70(HSP70)蛋白表达的角度观察井穴放血法对急性缺血性脑损伤的脑保护作用。[方法]以凝结法阻断大鼠一侧大脑中动脉造成急性局灶性缺血性脑损伤模型,用免疫组织化学法观察缺血区皮层脑组织HSP70蛋白的表达变化及施加井穴放血法后对其的干预作用。[结果]急性缺血性脑损伤可快速诱导HSP70蛋白在皮层缺血区脑组织的表达增加,其表达有随缺血时间延长逐渐增多的趋势,提示脑的缺血性损伤可应激性地增强神经细胞对缺血、缺氧的耐受和适应能力,而应用井穴放血的干预治疗可明显上调缺血区皮层脑组织HSP70的表达水平,进一步增强脑组织对抗缺血性损伤的应激能力,抵抗缺血性脑损害的进一步发展,增强脑修复能力。[结论]表明井穴放血法在中风早期可提高缺血区脑组织的抗应激能力,发挥出有效的脑保护作用。

[Objective] To observe the brain-protective effects of collateral puncture-bloodletting at JING point on the expression of HSP protein of brain in rats with acute local cerebral ischemia. [Methods] The cerebral injury with acute local ischemia was induced by occlusion of the middle cerebral artery with blood concretion in rats. The expression of HSP protein in ischemic region of brain tissue was determined with immunohistochemistry and the intervention of bloodletting at JING point was observed. [Result] Acute cerebral ishemic injury resulted in the expression of HSP protein in the ischemic region of brain tissue and this effect increased gradually with time. Bloodletting at JING point can enhance the expression of HSP protein in initial stage of ischemia and increase the resistance of brain against the exacerbation of the ischemic injury. [Conclusion] Bloodletting at JING point may improve the anti-stress ability of brain tissue in ischemic field and the protective function of the brain effectively.