司坦唑醇对体外培养的正常及白细胞介素-1β刺激的马软骨细胞的影响。
Effects of stanozolol on normal and IL-1β-stimulated equine chondrocytes in vitro.
作者信息
Castro Martins Mariana, Peffers Mandy J, Lee Katie, Rubio-Martinez Luis M
机构信息
Department of Equine Clinical Studies, Institute of Veterinary Science, University of Liverpool, Leahurst Campus, Chester High Road, Neston, CH64 7TE, UK.
Department of Musculoskeletal Biology, Institute of Ageing and Chronic Disease, University of Liverpool, Liverpool, UK.
出版信息
BMC Vet Res. 2018 Mar 20;14(1):103. doi: 10.1186/s12917-018-1426-z.
BACKGROUND
Intra-articular administration of stanozolol has shown promising results by improving the clinical management of lameness associated with naturally-occurring osteoarthritis (OA) in horses, and by decreasing osteophyte formation and subchondral bone reaction in sheep following surgically induced OA. However, there is limited evidence on the anti-inflammatory and modulatory properties of stanozolol on articular tissues. The objective of the current study was to evaluate the effects of stanozolol on chondrocyte viability and gene expression in normal equine chondrocytes and an inflammatory in vitro system of OA (interleukin-1β (IL-1β) treated chondrocytes).
RESULTS
Chondrocytes from normal metacarpophalangeal joints of skeletally mature horses were exposed to four treatment groups: (1) media only (2) media+IL-1β (3) media+IL-1β + stanozolol (4) media+stanozolol. Following exposure, chondrocyte viability and the expression of catabolic, anabolic and structural genes were determined. General linear models with Dunnet's comparisons with Bonferroni's adjustment were performed. Cell viability was similar in all groups. Stanozolol treatment reduced gene expression of MMP-13, MMP-1, IL-6 and COX-2 in both normal and IL-1β treated chondrocytes. Stanozolol treatment reduced ADAMTS4 gene expression in normal chondrocytes. Stanozolol reduced the expression of COL2A1.
CONCLUSIONS
The current study demonstrates stanozolol has chondroprotective effects through downregulation of genes for pro-inflammatory/catabolic cytokines and enzymes associated with OA. However, there is no evidence of increased cartilage stimulation through upregulation of the anabolic and structural genes tested.
背景
司坦唑醇关节内给药已显示出有前景的结果,它改善了与马自然发生的骨关节炎(OA)相关跛行的临床管理,并减少了手术诱导OA后绵羊的骨赘形成和软骨下骨反应。然而,关于司坦唑醇对关节组织的抗炎和调节特性的证据有限。本研究的目的是评估司坦唑醇对正常马软骨细胞以及OA炎症体外系统(白细胞介素-1β(IL-1β)处理的软骨细胞)中软骨细胞活力和基因表达的影响。
结果
将来自骨骼成熟马的正常掌指关节的软骨细胞暴露于四个处理组:(1)仅培养基;(2)培养基+IL-1β;(3)培养基+IL-1β+司坦唑醇;(4)培养基+司坦唑醇。暴露后,测定软骨细胞活力以及分解代谢、合成代谢和结构基因的表达。进行了带有Dunnet比较和Bonferroni校正的一般线性模型分析。所有组的细胞活力相似。司坦唑醇处理降低了正常和IL-1β处理的软骨细胞中MMP-13、MMP-1、IL-6和COX-2的基因表达。司坦唑醇处理降低了正常软骨细胞中ADAMTS4基因的表达。司坦唑醇降低了COL2A1的表达。
结论
本研究表明司坦唑醇通过下调与OA相关的促炎/分解代谢细胞因子和酶的基因而具有软骨保护作用。然而,没有证据表明通过上调所测试的合成代谢和结构基因而增加了软骨刺激。
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