BACKGROUND AND OBJECTIVE Osteoarthritis is the most common chronic osteoarthrosis disease. There are complex factors that lead to osteoarthritis. Therefore, it is essential to investigate the molecular mechanism of osteoarthritis, especially the mechanism of articular cartilage degeneration. In this study, the mechanism of FPR1 (formyl peptide receptor 1) in LPS (lipopolysaccharide) induced chondrogenic cell ATDC5 was investigated. MATERIALS AND METHODS We employed real-time quantitative polymerase chain reaction (RT-qPCR) and western blot assay to analyze the expression level of FPR1 in ATDC5 cell lines induced by LPS at 0, 2.5, 5, and 10 μg/mL concentrations. Then we constructed the FPR1 knockdown plasmid to transfect the LPS-ATDC5. MTT assay was used to test cell viability in control, LPS, LPS+shNC and LPS+shFPR1 groups. ELISA and RT-qPCR assay were employed to examine the TNF-α (tumor necrosis factor-α)ͿIL-6 and IL-1β expression level. Flow cytometry and western blot assay were employed to analyze the apoptosis of LPS-ATDC5. Finally, we utilized the western blot assay to text related protein expression level of MAPK (mitogen-activated protein kinase) signaling pathway. RESULTS In this study, we found the expression level of FPR1 was increased in LPS-ATDC5, downregulation of FPR1 improves the survival rate and alleviates inflammatory response of LPS-ATDC5. Meanwhile, downregulation of FPR1 alleviates apoptosis of LPS-ATDC5. Finally, downregulation of FPR1 inhibits the MAPK signal pathway. CONCLUSION Present study revealed that FPR1 was highly expressed in LPS-induced chondrocytes ATDC5, and the downregulation of FPR1 abated the inflammatory response and apoptosis of LPS-ATDC5 cells by regulating the MAPK signaling pathway.

中文翻译：

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FPR1的下调通过上调小鼠软骨形成ATDC5细胞中的MAPK信号通路减轻脂多糖诱导的炎症损伤和细胞凋亡。

背景和目的骨关节炎是最常见的慢性骨关节炎疾病。导致骨关节炎的因素很复杂。因此，研究骨关节炎的分子机制，尤其是关节软骨退变的机制是十分必要的。在这项研究中，研究了 FPR1（甲酰肽受体 1）在 LPS（脂多糖）诱导的软骨细胞 ATDC5 中的作用机制。材料与方法 我们采用实时定量聚合酶链反应 (RT-qPCR) 和蛋白质印迹法分析了 LPS 在 0、2.5、5 和 10 μg/mL 浓度下诱导的 ATDC5 细胞系中 FPR1 的表达水平。然后我们构建了 FPR1 敲低质粒来转染 LPS-ATDC5。MTT法用于测试对照、LPS、LPS+shNC和LPS+shFPR1组的细胞活力。ELISA和RT-qPCR测定用于检查TNF-α（肿瘤坏死因子-α）ͿIL-6和IL-1β表达水平。采用流式细胞术和蛋白质印迹法分析LPS-ATDC5的细胞凋亡。最后，我们利用蛋白质印迹法检测 MAPK（丝裂原活化蛋白激酶）信号通路的相关蛋白表达水平。结果在本研究中，我们发现LPS-ATDC5中FPR1的表达水平升高，FPR1的下调提高了存活率并减轻了LPS-ATDC5的炎症反应。同时，FPR1的下调减轻了LPS-ATDC5的凋亡。最后，FPR1 的下调抑制了 MAPK 信号通路。结论 目前的研究表明 FPR1 在 LPS 诱导的软骨细胞 ATDC5、