The Protection and Antioxidant Mechanisms of Corticosteroids in LPSTreated Retinal Pigment Epithelial Cells

Wang SJ, Yeh HC, Kao CL, Li HT, Li WJ, Liu SL, Chen CY
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Abstract

Dexamethasone (DEX) and triamcinolone acetonide (TA) are two corticosteroids as anti-inflammatory agents that have been used as an anti-inflammation in several diseases to protect against oxidative damage. The present study examined the anti?oxidant effect of DEX and TA on lipopolysaccharide (LPS)-induced intracellular reactive oxygen species (ROS) in human retinol epithelium ARPE-19 cells. DEX and TA markedly inhibited the LPSinduced intracellular ROS level. DEX and TA also inhibited the expression of NADPH oxidase subunit gp91 and p22. Moreover, the expression of two antioxidant enzymes, heme oxygenase-1 (HO-1) expression and gammaglutamylcysteine synthetase (gamma-GCS), were increased by DEX and TA treatment in LPS-treated ARPE-19 cells. These results indicate that DEX and TA inhibits the intracellular ROS response by blocking the NADPH oxidase pathway and may increase some antioxidant enzymes in LPS -induced ARPE-19 cells. Therefore, DEX and TA may be useful as antioxidant agents against oxidative damage in anti-inflammatory diseases.
皮质类固醇对lps处理视网膜色素上皮细胞的保护作用及抗氧化机制
地塞米松(Dexamethasone, DEX)和曲安奈德(triamcinolone acetonide, TA)是两种作为抗炎剂的皮质类固醇,在多种疾病中被用作抗炎剂,以防止氧化损伤。本研究考察了抗?DEX和TA对脂多糖(LPS)诱导的人视黄醇上皮ARPE-19细胞内活性氧(ROS)的氧化作用。DEX和TA显著抑制lps诱导的细胞内ROS水平。DEX和TA还能抑制NADPH氧化酶亚基gp91和p22的表达。DEX和TA处理后,lps处理的ARPE-19细胞中血红素加氧酶-1 (HO-1)和γ -谷氨酰胺半胱氨酸合成酶(γ - gcs)两种抗氧化酶的表达均增加。这些结果表明,DEX和TA通过阻断NADPH氧化酶途径抑制细胞内ROS反应,并可能增加LPS诱导的ARPE-19细胞中的某些抗氧化酶。因此,DEX和TA可能是抗炎疾病中抗氧化损伤的有效抗氧化剂。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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