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首页> 外文期刊>American Journal of Physiology >Glutathione regulates transforming growth factor-beta-stimulated collagen production in fibroblasts.
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Glutathione regulates transforming growth factor-beta-stimulated collagen production in fibroblasts.

机译：谷胱甘肽调节成纤维细胞中转化生长因子-β刺激的胶原蛋白的产生。

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摘要

Transforming growth factor-beta (TGF-beta) is a potent fibrogenic cytokine. The molecular mechanism underlying TGF-beta fibrogenesis, however, has not been completely elucidated. In this study, we showed that TGF beta decreased the intracellular GSH content in murine embryo fibroblasts (NIH 3T3), which was followed by an increase in collagen I mRNA content and collagen protein production. Prevention of GSH depletion with N-acetylcysteine (NAC), GSH, or GSH ester abrogated TGF-beta-stimulated collagen production, whereas a decrease in intracellular GSH content with L-buthionine-S,R-sulfoximine, an inhibitor of de novo GSH synthesis, enhanced TGF-beta-stimulated collagen production. These results suggest that GSH depletion induced by TGF-beta may mediate TGF-beta-stimulated collagen production. In addition, we showed that TGF-beta stimulated superoxide production and increased release of H2O2 from the cells, whereas GSH ester decreased basal and TGF-beta + glucose oxidase-stimulated H2O2 release. H2O2, exogenously added or continuously generated by glucose oxidase, enhanced TGF-beta-stimulated collagen production, whereas suppression of superoxide production by diphenyliodonium, an NAD(P)H oxidase inhibitor, blocked TGF-beta-stimulated collagen production. These data further suggest that reactive oxygen species are involved in TGF-beta-stimulated collagen production and that the effect of GSH depletion on TGF-beta-stimulated collagen production may be mediated by facilitating reactive oxygen species signaling.
机译：转化生长因子-β（TGF-β）是一种有效的纤维生成细胞因子。然而，尚未完全阐明TGF-β纤维发生的分子机制。在这项研究中，我们表明TGFβ降低了小鼠胚胎成纤维细胞（NIH 3T3）的细胞内GSH含量，其后胶原I mRNA含量和胶原蛋白产生增加。用N-乙酰半胱氨酸（NAC），GSH或GSH酯防止GSH耗竭，废除了TGF-β刺激的胶原蛋白生成，而新谷胱甘肽抑制剂L-buthionine-S，R-sulfoximine减少了细胞内GSH含量合成，增强了TGF-β刺激的胶原蛋白的产生。这些结果表明，TGF-β诱导的GSH耗竭可能介导TGF-β刺激的胶原蛋白产生。此外，我们发现TGF-β刺激了超氧化物的产生并增加了H2O2从细胞中的释放，而GSH酯则减少了基础和TGF-β+葡萄糖氧化酶刺激的H2O2释放。葡萄糖氧化酶外源添加或连续生成的H2O2增强了TGF-β刺激的胶原蛋白的产生，而NAD（P）H氧化酶抑制剂二苯碘鎓抑制超氧化物的产生则阻止了TGF-β刺激的胶原蛋白的产生。这些数据进一步表明，活性氧参与了TGF-β刺激的胶原蛋白的产生，而GSH耗竭对TGF-β刺激的胶原蛋白产生的影响可能是通过促进活性氧的信号传导来介导的。

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