【摘要】 目的　对氧自由基 (oxygenfreeradicals,OFRs)及其清除剂超氧化物歧化酶 (superoxidedis mutase ,SOD)在口腔粘膜炎性损害中的作用机制进行系统研究。方法　①建立OFRs致口腔粘膜急性炎症的动物模型 ,分别采用酶组织化学染色、组合导数分光光度法研究该损害中辅酶II黄递酶等酶活性以及氨基己糖、氨基葡萄糖水平的变化 ;②分别采用电子顺磁共振、放射免疫技术研究外源性SOD对该损害中OFRs及前列腺素E2 含量的影响。结果　①在动物模型损害中 ,辅酶II黄递酶等酶活性显著降低 ,氨基己糖和氨基葡萄糖水平显著升高 ;②在口腔粘膜局部注射SOD能使炎性损害中的OFRs相对含量以及前列腺素E2 水平明显降低。结论　①OFRs通过攻击上皮细胞内的重要酶类 ,使结缔组织中蛋白多糖分解 ,从而造成口腔粘膜组织的炎性损害 ;②SOD通过清除过量OFRs、减少炎症介质的产生而使炎性损害程度明显减轻。更多还原

【Abstract】 Objective To study the roles of oxygen free radicals (OFRs) and superoxide dismutase (SOD) in the inflammatory injury in animal oral mucosa Methods ① The animal model was established in which an acute oral mucosal inflammation was induced by OFRs Enzyme histological methods and biochemical methods were used respectively to investigate the activities of some important enzymes such as nicotinamide adenine dinucleotide phosphate diaphorase and the amount of aminohexoses in the lesions;②Electron spin resonance and radioimmunoassay were ultilize respectively to study the effects of exogenous SOD on the amount of OFRs and prostaglandin E 2(PGE 2) in the lesions Results ① The activities of the enzymes in the oral lesions decreased and the amount of aminohexoses increased significantly; ② Local administrating SOD could reduce the amount of OFRs and PGE 2 in the lesions sufficiently Conclusion OFRs induced the inflammatory lesion by injuring some important enzymes and connective tissues in the oral mucosa Local administrating SOD could scavenge OFRs and PGE 2 in the oral mucosa sufficiently and reduce the degree of OFRs——induced oral mucosal inflammatory injury更多还原