Osteoarthritis (OA), characterized by pain and stiffness, swelling, deformity and dysfunction of joints, affects large numbers of population. The purpose of this study was to discover the effects of taurine in human OA chondrocytes and explore the underlying mechanisms. 46 patients with different grades of OA were recruited. Of these patients, 24 underwent total knee replacement and cartilages were harvested. The mRNA expressions of type II collagen (Collagen II) and endoplasmic reticulum (ER) stress markers (GRP78, GADD153 and Caspase-12) in cartilages were quantified by qRT-PCR. Cell viability and apoptosis of patient-derived chondrocytes were assessed by the CCK-8 assay and flow cytometry assay, respectively. Meanwhile, protein levels of Collagen II and ER stress markers both in cartilages and chondrocytes were evaluated by Western blot. The mRNA and protein levels of Collagen II decreased as OA progressed, while the expressions of ER stress markers increased dramatically. H₂O₂ induced ER stress in chondrocytes, as shown by the significant increase in the expression of ER stress markers, inhibited chondrocyte viability and Collagen II synthesis, promoted apoptosis. However, taurine treatment inhibited these above phenomena. These results indicated that taurine exhibited anti-OA effect by alleviating H₂O₂ induced ER stress and subsequently inhibiting chondrocyte apoptosis.

骨关节炎（OA）的特征是疼痛和僵硬，肿胀，畸形和关节功能障碍，会影响大量人群。这项研究的目的是发现牛磺酸在人OA软骨细胞中的作用并探讨其潜在机制。招募了46例不同等级的OA患者。在这些患者中，有24位接受了全膝关节置换，并收获了软骨。通过qRT-PCR定量检测软骨中II型胶原蛋白（胶原II）和内质网（ER）应激标志物（GRP78，GADD153和Caspase-12）的mRNA表达。通过CCK-8分析和流式细胞术分别评估了患者来源的软骨细胞的细胞活力和凋亡。同时，通过蛋白质印迹法评估软骨和软骨细胞中胶原II和ER应激标志物的蛋白质水平。随着OA的进展，胶原蛋白II的mRNA和蛋白水平下降，而ER应激标志物的表达急剧增加。H₂ O ₂诱导软骨细胞内的ER应激，如ER应激标志物表达的显着增加所示，抑制了软骨细胞的活力和II型胶原的合成，促进了细胞凋亡。然而，牛磺酸治疗抑制了上述现象。这些结果表明，牛磺酸通过减轻H ₂ O ₂引起的ER应激并随后抑制软骨细胞凋亡而表现出抗OA作用。