中文摘要：

目的观察热敏灸对局灶性脑缺血再灌注损伤模型大鼠超氧化物歧化酶（SOD）的活性、表达和丙二醛（MDA）含量的影响，以阐明热敏灸减轻脑缺血再灌注损伤的作用机制。方法雄性sD大鼠36只，分为假手术组、模型组、艾灸组和热敏灸组。采用线栓法闭塞大脑中动脉2h后进行再灌注，制备局灶性脑缺血再灌注损伤模型；比色法测定SOD活性和MDA含量；Westernblot技术检测大鼠大脑皮质SOD2蛋白的表达。结果热敏灸组大鼠血清和大脑皮质SOD活性（22．78＋1．31）U／mL、（4909．6±1345．6）U／g均高于模型组（20．17±1．12）u，mL、（2602．0±1515．5）U／g，血清和大脑皮质MDA含量（3．78±2．oo）Izmol／L、（1226．5_＋38．4）nmol／g均低于模型组（16．82±6．70）／xmol／L、（1905．6±478．6）nmol／g；大脑皮质SOD2蛋白表达量（0．974＋0．166）高于模型组的（O．702±0．040）。结论热敏灸具有减轻大鼠脑缺血再灌注损伤的作用，提高SOD活性和表达、降低氧自由基含量可能是其作用机制之一。

英文摘要：

Objective To observe the effects of heat-sensitive moxibustion on the expression and activity of super- oxide dismutase （SOD） and the content of malondialdehyde （MDA） in focal cerebral ischemia-reperfusion injury in rats, and the mechanism thereof. Methods Thirty-six male SD rats were randomly divided into four groups, sham-operated group （n=6）, ischemia-reperfusion （I/R） injury group （n=10）, I/R injury with 15-minute moxibustion group （n=10） and I/R injury with 35-minute moxibustion group （n=10）. The focal cerebral ischemia-reperfusion rat model was induced by middle cere- bral artery occlusion （MCAO） for 2 h followed by reperfusion. Values of SOD activity and MDA content were determined by colorimetry, and the cortical expression of SOD2 protein was detected by Western blot technique. Results Values of SOD activities were significantly higher inserum （22.78＋ 1.31）U/mL and cortex （4 909.6＋ 1 345.6） U/g of heat-sensitive moxibus- tion group than those of model group （20.17＋ 1.12）U/mL and （2 602.0＋ 1 515.5）U/g. Values of MDA contents were significant- ly decreased in serum （3.78＋2.00） ~mol/L and cortex （1 226.5＋38.4）nmol/g in heat-sensitive moxibustion group than those of model group （16.82＋6.70） Ixmol/L and （1 905.6＋478.6） nmol/g. The cortical expression of SOD2 protein （0.974~0.166） was higher in heat-sensitive moxibustion group than that of model group （0.702_＋0.040）. Conclusion Heat-sensitive moxi- bustion could reduce the damage of cerebral inchemia-reperfusion, which might be through improving SOD activity, increas- ing SOD expression and decreasing MDA content.