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Sulforaphane suppresses cell growth and collagen expression of keloid fibroblasts

机译:萝卜硫素抑制细胞生长和胶原蛋白瘢痕疙瘩成纤维细胞的表达

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摘要

Keloids are fibroproliferative diseases characterized by the accumulation of an extracellular matrix including collagen. Various growth factors, or cytokines, and their receptors are overexpressed in keloids, and they are expected to be therapy targets. Sulforaphane, a dietary isothiocyanate, has recently shown anti-tumor, anti-inflammatory, and anti-fibrotic properties. In this study, we found that sulforaphane inhibited cell growth and reduced collagen at the mRNA and protein levels in keloid fibroblasts. Moreover, sulforaphane markedly suppressed the expression of IL-6 and -SMA and inhibited Stat3 and Smad3 signaling pathways in keloid fibroblast KF112 cells. Sulforaphane induced G2/M cell-cycle arrest with the induction of p21 in KF112 cells. In addition, sulforaphane inhibited cell growth and suppressed the expression of collagen in keloid fibroblasts under a coculture with peripheral blood mononuclear cells. Furthermore, sulforaphane suppressed IL-6, Stat3, and Smad3 signaling in the coculture system. This study suggests that sulforaphane may be a novel keloid treatment.
机译:瘢痕疙瘩是fibroproliferative疾病的积累细胞外基质包括胶原蛋白。生长因子、细胞因子及其受体在瘢痕疙瘩,他们是谁将治疗的目标。饮食异硫氰酸酯,最近所示抗肿瘤、抗炎和anti-fibrotic属性。萝卜硫素抑制细胞生长和减少胶原蛋白在瘢痕疙瘩的mRNA和蛋白水平成纤维细胞。抑制il - 6和sma的表达抑制Stat3和Smad3信号通路瘢痕疙瘩成纤维细胞KF112细胞。诱导G2 / M细胞循环逮捕与归纳KF112 p21的细胞。抑制细胞生长和抑制瘢痕疙瘩成纤维细胞胶原蛋白的表达在coculture外周血单核细胞。抑制il - 6, Stat3和Smad3信号coculture系统。萝卜硫素可能是一个新颖的瘢痕疙瘩治疗。

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