CAJ | 학술논문

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；Western blot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±2.00）μmol/L、（1226.5±38.4）nmol/g均低于模型组（16.82±6.70）μmol/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（0.702±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。
목적：관찰열민구대국조성뇌결혈재관주손상모형대서초양화물기화매（SOD）적활성、표체화병이철（MDA）함량적영향，이천명열민구감경뇌결혈재관주손상적작용궤제。방법웅성SD대서36지，분위가수술조、모형조、애구조화열민구조。채용선전법폐새대뇌중동맥2h후진행재관주，제비국조성뇌결혈재관주손상모형；비색법측정SOD활성화MDA함량；Western blot기술검측대서대뇌피질SOD2단백적표체。결과열민구조대서혈청화대뇌피질SOD활성（22.78±1.31）U/mL、（4909.6±1345.6）U/g균고우모형조（20.17±1.12）U/mL、（2602.0±1515.5）U/g，혈청화대뇌피질MDA함량（3.78±2.00）μmol/L、（1226.5±38.4）nmol/g균저우모형조（16.82±6.70）μmol/L、（1905.6±478.6）nmol/g；대뇌피질SOD2단백표체량（0.974±0.166）고우모형조적（0.702±0.040）。결론열민구구유감경대서뇌결혈재관주손상적작용，제고SOD활성화표체、강저양자유기함량가능시기작용궤제지일。
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 in serum (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)μmol/L and cortex (1 226.5±38.4)nmol/g in heat-sensitive moxibustion group than those of model group (16.82 ± 6.70)μmol/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.