眼炎症中的超氧化物:人和实验性葡萄膜炎

Mitsunori Yamada , Hitoshi Shichi , Takenosuke Yuasa , Yoshihito Tanouchi , Yasuo Mimura
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引用次数: 22

摘要

研究了超氧化物在人类和实验动物的葡萄膜炎症发病机制中的可能参与。白塞患者的白细胞产生超氧化物在发作期明显高于缓解期。s抗原诱导的实验性自身免疫性葡萄膜视网膜炎(EAU)豚鼠白细胞超氧化物生成也增强。如果动物在EAU发作时给予超氧化物歧化酶(SOD)处理,房水细胞计数明显低于对照组(即未给予SOD处理)。在sod处理的动物中,前视网膜炎症细胞的浸润明显减少。在兔血清白蛋白诱导的被动Arthus型葡萄膜炎中也观察到SOD对组织损伤的类似保护作用。这些结果表明,超氧化物可能在眼部炎症动物模型中引起组织损伤,并可能在Behcet病中起作用。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Superoxide in ocular inflammation: Human and experimental uveitis

A possible involvement of Superoxide in the pathogenesis of uveal inflammation in man and experimental animals was investigated. Superoxide production by the leukocytes of Behcet patients was significantly higher in the attack phase than in the remission phase. Leukocyte Superoxide generation was also enhanced in guinea pigs with S-antigen-induced experimental autoimmune uveoretinitis (EAU). If the animals were treated with Superoxide dismutase (SOD) at the onset of EAU, aqueous humor cell count was significantly lower than that of control (i.e., without SOD treatment). Infiltration of the inflammatory cells in the anterior retina was markedly reduced in SOD-treated animals. A similar protective effect of SOD against tissue damage was also observed in a bovine serum albumin-induced passive Arthus type uveitis in rabbits. These results suggest that Superoxide may play a role in causing tissue damage in animal models of ocular inflammation and possibly in Behcet disease.

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