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首页> 外文期刊>Journal of Cellular Physiology >Sulforaphane protects human chondrocytes against cell death induced by various stimuli.
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Sulforaphane protects human chondrocytes against cell death induced by various stimuli.

机译：萝卜硫素保护人类软骨细胞各种刺激引起的细胞死亡。

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摘要

Chondrocyte cell death can contribute to cartilage degeneration in articular diseases, such as osteoarthritis (OA). Sulforaphane (SFN), a natural compound derived from cruciferous aliment, is well known as an anti-carcinogen, but according to recent evidence it also shows cytoprotective effects on a variety of non-tumoral cells. Therefore we have tested the ability of SFN to protect chondrocytes from cell death in vitro. Treatment of growing monolayer cultures of human C-28/I2 chondrocytes with SFN in the low micro-molecular range for a few days, reduced cell growth without affecting cell survival or inducing apoptosis. However it decreased cell death in C-28/I2 chondrocytes exposed to stimuli previously reported to promptly trigger apoptosis, that is, the cytokine tumor necrosis factor-alpha (TNF) plus cycloheximide (CHX) or the polyamine analogue N(1),N(11)-diethylnorspermine (DENSPM) plus CHX. In particular pre-treatment with SFN reduced effector and initiator caspase activities and the associated activation of JNK kinases. SFN exerted a cytoprotective action even versus H(2)O(2) , which differently from the previous stimuli induced cell death without producing an evident caspase activation. SFN pre-treatment also prevented caspase activation in three-dimensional micromass cultures of OA chondrocytes stimulated with growth-related oncogene alpha (GROalpha), a pro-apoptotic chemokine. The suppression of caspase activation in micromasses appeared to be related to the inhibition of p38 MAPK phosphorylation. In conclusion, the present work shows that low micro-molecular SFN concentrations exert pro-survival and anti-apoptotic actions and influence signaling pathways in a variety of experimental conditions employing chondrocyte cell lines and OA chondrocytes treated with a range of death stimuli.
机译：软骨细胞细胞死亡可以促进软骨退化的关节疾病,如骨关节炎(OA)。天然化合物来自十字花科滋养品,众所周知作为一种抗癌物质,但是根据最近的证据也显示对各种cytoprotective影响non-tumoral细胞。SFN保护软骨细胞免受细胞的能力死亡在体外。人类C-28 / I2软骨细胞与SFN的文化在低micro-molecular范围内几天,减少细胞生长而不影响细胞生存或诱导细胞凋亡。减少细胞死亡在C-28 / I2软骨细胞暴露在刺激之前报道立即引发细胞凋亡,细胞因子肿瘤坏死因子-α(TNF) +环己酰亚胺(CHX)或聚胺类似物N (1), (11) -diethylnorspermine (DENSPM) + CHX。特别是预处理与SFN减少效应和引发剂和半胱天冬酶的活动物激酶的活化有关。cytoprotective行动甚至与H (2) O (2),不同于之前的刺激没有产生明显的诱导细胞死亡半胱天冬酶激活。避免在三维半胱天冬酶的激活micromass文化OA软骨细胞的刺激与成长相关癌基因的α(GROalpha)pro-apoptotic趋化因子。半胱天冬酶激活micromasses似乎p38 MAPK的抑制有关磷酸化。表明低micro-molecular SFN浓度发挥pro-survival和抗凋亡的行为信号通路的影响实验条件采用软骨细胞细胞系和OA软骨细胞治疗范围死亡的刺激。

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