Cui Luping, Han Yongbin, Dong Zhijie
Department of Rheumatology and Immunology, Shanxi Provincial People's Hospital, Taiyuan, Shanxi Province, China.
Department of Orthopedics, The First Hospital of Shan Xi Medical University, Taiyuan, Shanxi Province, China.
Arch Med Sci. 2020 Feb 2;20(1):302-308. doi: 10.5114/aoms.2020.92831. eCollection 2024.
Osteoarthritis (OA) is a common inflammatory joint disease characterised by progressive cartilage destruction. Management of this condition remains a significant challenge, and new therapies are required. We investigated the protective effects of miR-106a mimics in a murine model of OA.
This study was performed using both and OA models. Primary chondrocytes were isolated from female rats, with inflammation induced via treatment with lipopolysaccharide (LPS). Then the effects of a miR-106a mimic were examined based on the level of inflammatory cytokine production and apoptotic signalling following LPS stimulation. An rat model of OA was generated by injecting LPS into the anterior cruciate ligament, followed by treatment with miR-106a mimics. Then, inflammatory and apoptotic protein expression was assessed in the cartilage tissue.
Treatment with miR-106a mimic reduced the levels of inflammatory cytokines and apoptotic proteins in cartilage tissues following LPS-induced inflammation. Furthermore, the mimic ameliorated the expression of DR-6 mRNA and DR6, IκBα, and p65 proteins in chondrocytes. Similar effects were seen in the model, with the mimic attenuating expression of NF-κB, p65, IκBα, and DR6 proteins and improving histopathological outcomes in the chondrocytes of OA rats.
Treatment with miR-106a mimic ameliorates inflammation in cartilage tissues of OA subjects by activating death receptor 6 via the NF-κB signalling pathway.
骨关节炎（OA）是一种常见的炎症性关节疾病，其特征为软骨进行性破坏。对这种疾病的治疗仍然是一项重大挑战，因此需要新的治疗方法。我们研究了miR-106a模拟物在OA小鼠模型中的保护作用。
本研究使用了[未提及具体模型名称]和OA模型。从雌性大鼠中分离出原代软骨细胞，通过脂多糖（LPS）处理诱导炎症。然后根据LPS刺激后炎症细胞因子产生水平和凋亡信号来检测miR-106a模拟物的作用。通过将LPS注射到前交叉韧带中建立大鼠OA模型，随后用miR-106a模拟物进行治疗。然后，评估软骨组织中炎症和凋亡蛋白的表达。
用miR-106a模拟物治疗可降低LPS诱导炎症后软骨组织中炎症细胞因子和凋亡蛋白的水平。此外，该模拟物改善了软骨细胞中DR-6 mRNA以及DR6、IκBα和p65蛋白的表达。在[未提及具体模型名称]模型中也观察到了类似的效果，该模拟物可减弱OA大鼠软骨细胞中NF-κB、p65、IκBα和DR6蛋白的表达，并改善组织病理学结果。
用miR-106a模拟物治疗可通过NF-κB信号通路激活死亡受体6来减轻OA患者软骨组织中的炎症。
