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镉对白色来亨鸡胚胎软骨细胞的毒性及 1α,25 - 二羟基维生素 D 的缓解作用

Cadmium Toxicity on Chondrocytes and the Palliative Effects of 1α, 25-Dihydroxy Vitamin D in White Leghorns Chicken's Embryo.

作者信息

Gu Jianhong, Li Saihui, Wang Guoshuai, Zhang Xueqing, Yuan Yan, Liu Xuezhong, Bian Jianchun, Tong Xishuai, Liu Zongping

机构信息

College of Veterinary Medicine, Yangzhou University, Yangzhou, China.

Jiangsu Co-innovation Center for Prevention and Control of Important Animal Infectious Diseases and Zoonoses, Yangzhou, China.

出版信息

Front Vet Sci. 2021 Feb 10;8:637369. doi: 10.3389/fvets.2021.637369. eCollection 2021.

Abstract

Cadmium (Cd) can causes osteoporosis and joint swelling. However, the mechanism of Cd toxicity in chondrocytes and how to alleviate Cd poisoning to chondrocytes are still unclear. Herein, we evaluated the toxicity of Cd to chicken chondrocytes, and whether vitamin D can relieve the toxicity of Cd to chondrocytes. Primary chondrocytes were collected from knee-joint cartilage of 15-day-old chicken embryos. They were treated with (0, 1, 2, and 4) μM Cd alone, 10 M 1α,25-(OH)D alone, or 2 μM Cd combined with 10 M 1α,25-(OH)D. We found that Cd significantly inhibited and mRNA expression, which are markers for chondrocyte differentiation, downregulated the mitochondrial membrane potential, upregulated the Bax/B-cell lymphoma 2 ratio. Furthermore, Cd significantly promoted matrix metalloproteinase (MMP)-9 expression, thus accelerating the degradation of extracellular matrix. And Cd also inhibited the expression of main macromolecular protein of extracellular matrix, Collagen type IIα1 (COL2A1) and acid mucopolysaccharide. However, 1α,25-(OH)D pretreatment significantly alleviated the toxicity effects of Cd on the differentiation, apoptosis and extracellular matrix gene expression in primary chondrocytes. Conclusively, Cd exposure could inhibited chicken embryo chondrocytes differentiation, extracellular matrix gene expression, and induced chondrocyte apoptosis. However, these toxic effects of Cd are alleviated by the pretreatment of chondrocytes with 1α,25-(OH)D.

摘要

镉(Cd)可导致骨质疏松和关节肿胀。然而,Cd对软骨细胞的毒性机制以及如何减轻Cd对软骨细胞的中毒作用仍不清楚。在此,我们评估了Cd对鸡软骨细胞的毒性,以及维生素D是否能减轻Cd对软骨细胞的毒性。从15日龄鸡胚的膝关节软骨中收集原代软骨细胞。它们分别用(0、1、2和4)μM的Cd单独处理、10 nM的1α,25-(OH)D单独处理,或2 μM的Cd与10 nM的1α,25-(OH)D联合处理。我们发现,Cd显著抑制了作为软骨细胞分化标志物的 和 mRNA表达,下调了线粒体膜电位,上调了Bax/B细胞淋巴瘤-2比值。此外,Cd显著促进基质金属蛋白酶(MMP)-9的表达,从而加速细胞外基质的降解。并且Cd还抑制了细胞外基质主要大分子蛋白Ⅱ型胶原α1(COL2A1)和酸性粘多糖的表达。然而,1α,25-(OH)D预处理显著减轻了Cd对原代软骨细胞分化、凋亡和细胞外基质基因表达的毒性作用。总之,Cd暴露可抑制鸡胚软骨细胞分化、细胞外基质基因表达,并诱导软骨细胞凋亡。然而,用1α,25-(OH)D预处理软骨细胞可减轻Cd的这些毒性作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d738/7902530/62c392155385/fvets-08-637369-g0001.jpg

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