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首页> 外文期刊>Journal of cellular physiology. >Inhibiting the aberrant activation of Wnt/p-catenin signaling by selenium supplementation ameliorates deoxynivalenol-induced toxicity and catabolism in chondrocytes
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Inhibiting the aberrant activation of Wnt/p-catenin signaling by selenium supplementation ameliorates deoxynivalenol-induced toxicity and catabolism in chondrocytes

机译：抑制的异常激活硒Wnt / p-catenin信号补充改善了deoxynivalenol-induced毒性和分解代谢软骨细胞

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摘要

Kashin-Beck disease (KBD) is an endemic degenerative osteoarticular disorder associated with physical disability and a heavy economic burden. Contamination by mycotoxin deoxynivalenol (DON) and selenium deficiency have been proposed to be key etiological factors for KBD, and can work together to aggravate the progression of KBD. Nevertheless, the mechanism of DON in KBD remains elusive. In the present study, exposure to DON dose-dependently suppressed cell viability and expression of pro-proliferation marker PCNA in human chondrocytes, whereas it enhanced lactate dehydrogenase release, cell apoptosis, and caspase-3/9 activity. In addition, DON incubation shifted metabolism homeostasis towards catabolism by suppressing the transcription of collagen II and aggrecan, and the production of sulphated glycosami-noglycans and TIMP-1, while increasing matrix metalloproteinase levels (MMP-1 and MMP-13). Mechanistically, DON exposure induced the activation of Wnt/β-catenin signaling. Intriguingly, blocking this pathway reversed the adverse effects of DON on cytotoxic damage and metabolism disruption to catabolism. Notably, supplementation with selenium reduced DON-induced activation of the Wnt/β-catenin pathway. Moreover, selenium addition abrogated cytotoxic injury and excessive pro-catabolic gene expression in chondrocytes upon DON conditions. These findings confirm that DON may facilitate the development of KBD by inducing cell injury, inhibiting matrix synthesis, and increasing cellular catabolism by activating the Wnt/β-catenin signaling, which were partially reversed by selenium supplementation. Thus, the current study may presents a new viewpoint for how selenium supplementation ameliorates the development of KBD by inhibiting DON-induced cytotoxic injury and metabolism imbalance in chondrocytes.
机译：大骨节病(KBD)是一种流行退行性osteoarticular紊乱相关身体残疾和沉重的经济负担。(唐)和硒缺乏症关键KBD的病因学因素,可以共同努力,加剧的发展KBD。仍然是难以捉摸的。可剂量依赖性抑制细胞的生存能力和pro-proliferation标记PCNA的表达在人类软骨细胞,而增强乳酸脱氢酶释放,细胞凋亡,和caspase-3/9活动。孵化转移代谢体内平衡分解代谢的抑制转录胶原蛋白II和aggrecan和生产硫酸化glycosami-noglycans TIMP-1,增加基质金属蛋白酶(金属蛋白酶- 1的水平和MMP-13)。诱导激活Wnt /β连环蛋白信号。逆转的不利影响并在细胞毒性损伤和破坏分解代谢。值得注意的是,补充硒降低DON-induced激活Wnt /β连环蛋白途径。细胞毒性损伤和过度pro-catabolic基因在软骨细胞在条件表达式。这些发现证实,并可能促进KBD的诱导细胞损伤的发展,抑制矩阵合成,增加通过激活细胞分解代谢Wnt /β连环蛋白信号部分逆转了硒的补充。目前的研究提出了一种新的观点硒的补充改善如何通过抑制DON-induced KBD的发展细胞毒性损伤和代谢失衡软骨细胞。

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