Institute of Endemic Diseases, School of Medicine, Xi'an Jiaotong University, Xi'an 710061, China.
J Zhejiang Univ Sci B. 2010 Mar;11(3):200-8. doi: 10.1631/jzus.B0900074.
To investigate the effects of mycotoxin moniliformin (MON) on the metabolism of aggrecan and type II collagen in human chondrocytes in vitro and the relationship between MON and Kashin-Beck disease (KBD).
Human chondrocytes were isolated and cultured on bone matrix gelatin to form an artificial cartilage model in vitro with or without MON toxin. Cell viability was determined by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay. The expression of aggrecan and type II collagen in the cartilage was determined using immunocytochemical staining.
MON toxin inhibited chondrocyte viability in dose-dependent and time-dependent manners. MON reduced aggrecan and type II collagen syntheses in the tissue-engineered cartilage. MON also increased the expression of matrix metalloproteinase-1 (MMP-1), MMP-13, BC4 epitopes, and CD44 in cartilages. However, the expression of 3B3(-) epitopes in cartilages was inhibited by MON. Selenium partially alleviated the damage of aggrecan induced by MON toxin.
MON toxin promoted the catabolism of aggrecan and type II collagen in human chondrocytes.
研究真菌毒素玉米赤霉烯酮(MON)对体外人软骨细胞中聚集蛋白聚糖和 II 型胶原代谢的影响,以及 MON 与大骨节病(KBD)的关系。
采用骨基质明胶体外培养人软骨细胞,构建人工软骨模型,分别加入或不加入 MON 毒素。通过 3-(4,5-二甲基噻唑-2-基)-2,5-二苯基四氮唑溴盐(MTT)比色法检测细胞活力。免疫细胞化学染色法检测软骨中聚集蛋白聚糖和 II 型胶原的表达。
MON 毒素呈剂量和时间依赖性抑制软骨细胞活力。MON 减少组织工程软骨中聚集蛋白聚糖和 II 型胶原的合成。MON 还增加了软骨中基质金属蛋白酶-1(MMP-1)、MMP-13、BC4 表位和 CD44 的表达,但抑制了软骨中 3B3(-)表位的表达。硒部分缓解了 MON 毒素诱导的聚集蛋白聚糖损伤。
MON 毒素促进了人软骨细胞中聚集蛋白聚糖和 II 型胶原的分解代谢。