LncRNA myocardial infarction associated transcript (MIAT) has been shown to be involved in osteoarthritis (OA), but its role in Kashin-Beck Disease (KBD) has rarely been reported. In this study, rats were administered with low selenium and/or T-2 toxin for 4 weeks to establish a KBD animal model. The serum selenium level, TNF-α and IL-1β contents, phosphorylated p65 (p-p65) and MIAT expression were increased in each intervention group. Next, we isolated the primary epiphyseal chondrocytes, and found that selenium treatment reversed the effects of T-2 toxin on chondrocyte injury, p-p65 and MIAT expression. In addition, MIAT overexpression or T-2 toxin treatment led to increased cell death, apoptosis, inflammation, NF-κB-p65 pathway activation and MIAT expression, which was rescued by selenium treatment or MIAT siRNA transfection. Our results suggested that lncRNA MIAT regulated by selenium and T-2 toxin increased the activation of NF-κB-p65, thus being involved in the progress of KBD.

LncRNA 心肌梗死相关转录物 (MIAT) 已被证明与骨关节炎 (OA) 相关，但其在大骨节病 (KBD) 中的作用却鲜有报道。在这项研究中，大鼠被给予低硒和/或T-2毒素4周以建立KBD动物模型。各干预组血清硒水平、TNF-α和IL-1β含量、磷酸化p65（p-p65）和MIAT表达均升高。接下来，我们分离了初级骨骺软骨细胞，发现硒处理逆转了 T-2 毒素对软骨细胞损伤、p-p65 和 MIAT 表达的影响。此外，MIAT 过表达或 T-2 毒素处理导致细胞死亡、细胞凋亡、炎症、NF-κB-p65 通路激活和 MIAT 表达增加，这通过硒处理或 MIAT siRNA 转染得以挽救。