Suppression of S antigen-induced uveitis by vitamin E supplementation.
Suppression of S antigen-induced uveitis by vitamin E supplementation.
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通过补充维生素 E 抑制 S 抗原诱导的葡萄膜炎。
DOI：
10.1159/000267110
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发表时间：
1991
影响因子：
2.1
通讯作者：
Rao,NA
中科院分区：
文献类型：
--
作者：
Pararajasegaram,G;Sevanian,A;Rao,NA
使用葡萄膜视网膜炎的S抗原模型研究维生素E的抗炎作用。将36只3周龄刘易斯大鼠分成3组，并维持特殊配制的饮食。一组动物接受缺乏维生素E的饮食;第二组接受含有维生素E的正常饮食;第三组除了接受正常饮食外，还接受维生素E补充剂。在9周龄时，所有大鼠均对S抗原致敏。在免疫后第14天处死每组中的6只动物，并在第21天处死剩余动物。进行了组织病理学和生化研究，以评估在维持不同维生素饮食水平的动物中观察到的组织损伤。补充维生素E组的眼内炎症明显小于其他两组（p < 0.01）。前一组的眼睛和血浆中的维生素E水平最高（平均值分别为1.13 µg/mg蛋白质和23.9 µg/ml），而维生素E缺乏组的水平最低（眼睛和血浆中的平均值分别为0.16 µg/mg蛋白质和0.48 µg/ml）。花生四烯酸代谢产物的放射免疫测定结果显示，维生素E补充组血栓素B2水平（2.04 ± 0.45 pg/mg）明显低于正常组（4.33 ± 0.98 pg/mg）和维生素E缺乏组（5.21 ± 1.12 pg/mg）（P < 0.01）。我们的研究结果表明，膳食补充维生素E导致减少花生四烯酸代谢产物，眼部炎症和视网膜损伤引起的视网膜S抗原。
The anti-inflammatory effects of vitamin E were investigated using the S antigen model of uveoretinitis. Thirty-six 3-week-old Lewis rats were separated into three groups and maintained on a specially formulated diet. One group of animals received a diet deficient in vitamin E; a second group received a normal diet containing vitamin E, and the third group, in addition to receiving the normal diet, received vitamin E supplementation. At 9 weeks of age, all rats were sensitized to S antigen. Six animals in each group were killed on day 14 and the remaining animals on day 21 following immunization. Both histopathologic and biochemical studies were conducted to evaluate the tissue damage observed in animals maintained on different dietary levels of the vitamin. The intraocular inflammation in the vitamin E-supplemented group was considerably smaller than in the other two groups (p < 0.01). The former group had the highest level of vitamin E in both the eye and plasma (mean value 1.13 µg/mg protein and 23.9 µg/ml, respectively), while the vitamin E-deficient group had the lowest levels (mean values of 0.16 µg/mg protein and 0.48 µg/ml in the eye and plasma, respectively). Results of the radioimmunoassay for the determination of the arachidonic acid metabolites revealed significantly lower levels of thromboxane B2in the vitamin E-supplemented group (2.04 ± 0.45 pg/mg) than in the normal (4.33 ± 0.98 pg/mg) or the vitamin E-deficient (5.21 ± 1.12 pg/mg) groups (p < 0.01). Our results indicate that dietary supplementation with vitamin E causes a reduction in the arachidonic acid metabolites, ocular inflammation and retinal damage induced by retinal S antigen.