Guangxi Engineering Center in Biomedical Materials for Tissue and Organ Regeneration, The First Affiliated Hospital of Guangxi Medical University, Nanning, Guangxi, China (mainland).
Guangxi Collaborative Innovation Center for Biomedicine, The First Affiliated Hospital of Guangxi Medical University, Nanning, Guangxi, China (mainland).
Med Sci Monit. 2018 Jan 27;24:539-547. doi: 10.12659/msm.907969.
BACKGROUND Worldwide, femoral head necrosis (FHN), which is also known as avascular necrosis of the femoral head or osteonecrosis of the femoral head, affects millions of people. Excess alcohol intake and steroid use are two common associations with FHN, but their pathogenesis remains unknown. The aim of this study was to develop an in vitro model using human chondrocytes to study alcohol-induced and steroid-induced FHN. MATERIAL AND METHODS In this study, the in vitro model used a monolayer culture of articular chondrocytes derived from patients with non-traumatic FHN (Ficat and Arlet, Stage III). Normal chondrocytes were obtained from patients with femoral neck fracture resulting from road traffic accident (Garden, Stage IV). Alcohol-stimulated and steroid-stimulated articular chondrocytes were evaluated by a cell proliferation assay, measurement of calcium levels (alizarin red), measurement of alkaline phosphatase (ALP) levels, detection of glycosaminoglycan (GAG) secretion using safranin O histochemical staining, and analysis of cartilage-specific genes, ACAN, SOX9, OPG, TGF-β, RANKL, and RUNX2, using quantitative real-time polymerase chain reaction (qRT-PCR). RESULTS Both alcohol and steroids, but especially steroids, accelerated the degradation of cartilage by suppression of chondrogenesis while promoting chondrocyte hypertrophy and activating osteogenic differentiation, as assessed by cell proliferation assay, detection of glycosaminoglycan (GAG) secretion, and analysis of cartilage-specific genes. CONCLUSIONS A human chondrocyte-derived in vitro model of alcohol-induced and steroid-induced FHN demonstrated chondrocyte hypertrophy and activated osteogenic differentiation.
在全球范围内，股骨头坏死（FHN），也称为股骨头缺血性坏死或股骨头坏死，影响着数百万人。过量饮酒和使用类固醇是与 FHN 相关的两个常见因素，但它们的发病机制仍不清楚。本研究旨在建立一种使用人软骨细胞的体外模型，以研究酒精诱导和类固醇诱导的 FHN。
在这项研究中，体外模型使用了来自非创伤性 FHN 患者（Ficat 和 Arlet，III 期）的关节软骨单层培养。正常软骨细胞取自因道路交通意外导致股骨颈骨折的患者（Garden，IV 期）。通过细胞增殖测定、钙水平（茜素红）测定、碱性磷酸酶（ALP）水平测定、软骨特异性基因 ACAN、SOX9、OPG、TGF-β、RANKL 和 RUNX2 的定量实时聚合酶链反应（qRT-PCR）分析，评估酒精刺激和类固醇刺激的关节软骨细胞。
酒精和类固醇都能加速软骨的降解，抑制软骨生成，同时促进软骨细胞肥大和激活成骨分化，这通过细胞增殖测定、糖胺聚糖（GAG）分泌检测和软骨特异性基因分析得到了证实。
从人软骨细胞中建立的酒精诱导和类固醇诱导的 FHN 体外模型显示出软骨细胞肥大和激活的成骨分化。
