1α,25(OH)_2D_3调控关节软骨Ⅱ型胶原降解的实验研究

1α,2525(OH)_2D_3regulates degradation of type Ⅱ collagen in articular cartilage

背景背景:维生素D代谢水平与关节炎的关系仍存在争议,且维生素D对关节软骨Ⅱ型胶原代谢的调控机制尚不明晰。深入了解维生素D对骨关节炎软骨代谢的作用,有助于了解骨关节炎的病因及发病机制,为预防、治疗骨关节炎提供参考。目的目的:在细胞水平和组织块水平,探讨维生素D对关节软骨Ⅱ型胶原代谢的调控作用。方法方法:使用炎症因子OSM和TNF-α诱导软骨Ⅱ型胶原降解,对大鼠关节软骨细胞以及牛关节软骨组织块分别进行1α,25(OH)2D3干预,通过ELISA检测细胞上清中Ⅱ型胶原羧基末端肽(CTX-Ⅱ)水平,从而评估维生素D对软骨Ⅱ型胶原代谢的调控作用。结果结果:1α,25(OH)2D3可以提高未经OSM和TNF-α诱导的以及OSM和TNF-α诱导后的软骨细胞的活性。在细胞水平,1α,25(OH)2D3对正常细胞上清中的CTX-Ⅱ的水平没有显著影响。OSM和TNF-α诱导显著增加了细胞上清中CTX-Ⅱ的水平。1α,25(OH)2D干预降低了OSM和TNF-α诱导的软骨细胞上清中CTX-Ⅱ的水平。在组织块水平,对于正常软骨组织块,1α,25(OH)2D3增加了CTX-Ⅱ水平。OSM和TNF-α诱导显著增加了体外培养关节软骨组织块软骨的降解,细胞上清中CTX-Ⅱ水平显著增高。对于OSM和TNF-α诱导的软骨组织块,1α,25(OH)2D3干预降低了软骨组织块Ⅱ胶原的降解,CTX-Ⅱ水平显著降低。结论结论:1α,25(OH)2D3能够抑制OSM和TNF-α诱导的Ⅱ型胶原降解作用。维生素D可能通过抑制关节炎软骨的降解起到保护关节软骨的作用。

Background：Disagreement on the relationship between vitamin D metabolism and osteoarthritis （OA） still exists in the liter-atures. Investigating the role of vitamin D in OA cartilage metabolism will help to well understand the etiology and patho-genesis of OA, and will contribute to improvement in the prevention and treatment of OA. Objective：To investigate the modulation of vitamin D on collagen typeⅡdegradation at cell and tissue levels. Methods：Rat articular chondrocytes and bovine articular cartilage explants were stimulated by inflammatory factors （OSM and TNF-α） to imitate OA cartilage chondrocytes, then were treated by 1α,25（OH）2D3. C terminal fragments of typeⅡcolla-gen （CTX-Ⅱ） expression in supernatant was measured by ELISA to evaluate degradation of collagenⅡ. Results：At cellular level, the combined effects of OSM and TNF-αincreased CTX-Ⅱ level in supernatant. 1α,25（OH）2D3 decreased the CTX-Ⅱ level which was induced by OSM plus TNF-α. At the tissue level, the stimulation of OSM plus TNF-αincreased CTX-Ⅱ level in the supernatant. 1α,25（OH）2D3 increased the CTX-Ⅱ levels in the normal cartilage tissue. 1α,25 （OH）2D3 decreased CTX-Ⅱlevels in cartilage tissue with OSM plus TNF-αstimulation. Conclusions： 1α,25（OH）2D3 can inhibit the degradation of collagen Ⅱ in articular chondrocytes stimulated by OSM plus TNF-α. Vitamin D may play a protective role in articular cartilage through regulation of cartilage turnover.