Abstract C1q/TNF-related protein 9 (CTRP9), the closest paralog of adiponectin, has been reported to protect against inflammation-related diseases. However, its role in regulating osteoarthritis (OA) has not been fully elucidated. First, a rat model of OA was generated. Furthermore, rats with OA were injected with different doses of recombinant CTRP9 protein (rCTRP9), and the knee cartilage damage was evaluated. Finally, the phosphorylation of p38 and the secretion of matrix metalloproteinases (MMPs) were detected by Western blotting and enzyme-linked immunosorbent assay. Results revealed that CTRP9 was highly expressed in adipose tissue, followed by skeletal muscle and cartilage tissue, and less expressed in liver, kidney and lung. Moreover, the expression of CTRP9 significantly decreased in the monosodium iodoacetate (MIA) group in the knee cartilage and knee synovial fluid, and the contents of interleukin-1β (IL-1β) and IL-6 significantly increased in knee synovial fluid. In addition, rCTRP9 alleviated MIA-induced inflammation, oxidative stress and knee cartilage damage in a dose-dependent way. In addition, rCTRP9 could attenuate the expression of p38MAPK and p-p38 and suppress the expression of nuclear factor-kappa B (NF-κB), p65 and MMPs. Collectively, the results of the present study suggested that CTRP9 alleviates the inflammation of MIA-induced OA through deactivating p38MAPK and NF-κB signaling pathways in rats.

中文翻译：

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CTRP9通过使骨关节炎大鼠的MAPK/NF-κB通路失活来防止MIA诱导的炎症和膝关节软骨损伤

摘要 C1q/TNF 相关蛋白 9 (CTRP9) 是脂联素最接近的旁系同源物，据报道可预防炎症相关疾病。然而，其在调节骨关节炎（OA）中的作用尚未完全阐明。首先，生成OA大鼠模型。此外，OA大鼠注射不同剂量的重组CTRP9蛋白（rCTRP9），评估膝关节软骨损伤。最后，通过蛋白质印迹和酶联免疫吸附试验检测 p38 的磷酸化和基质金属蛋白酶 (MMPs) 的分泌。结果显示，CTRP9在脂肪组织中高表达，其次是骨骼肌和软骨组织，在肝、肾和肺中表达较少。而且，CTRP9在碘乙酸钠（MIA）组膝关节软骨和膝关节滑液中的表达显着降低，膝关节滑液中白细胞介素-1β（IL-1β）和IL-6的含量显着增加。此外，rCTRP9 以剂量依赖性方式减轻 MIA 诱导的炎症、氧化应激和膝关节软骨损伤。此外，rCTRP9 可以减弱 p38MAPK 和 p-p38 的表达，并抑制核因子-κB (NF-κB)、p65 和 MMPs 的表达。总的来说，本研究的结果表明 CTRP9 通过使大鼠的 p38MAPK 和 NF-κB 信号通路失活来减轻 MIA 诱导的 OA 的炎症。rCTRP9 以剂量依赖性方式减轻 MIA 诱导的炎症、氧化应激和膝关节软骨损伤。此外，rCTRP9 可以减弱 p38MAPK 和 p-p38 的表达，并抑制核因子-κB (NF-κB)、p65 和 MMPs 的表达。总的来说，本研究的结果表明 CTRP9 通过使大鼠的 p38MAPK 和 NF-κB 信号通路失活来减轻 MIA 诱导的 OA 的炎症。rCTRP9 以剂量依赖性方式减轻 MIA 诱导的炎症、氧化应激和膝关节软骨损伤。此外，rCTRP9 可以减弱 p38MAPK 和 p-p38 的表达，并抑制核因子-κB (NF-κB)、p65 和 MMPs 的表达。总的来说，本研究的结果表明 CTRP9 通过使大鼠的 p38MAPK 和 NF-κB 信号通路失活来减轻 MIA 诱导的 OA 的炎症。