CCR5 silencing reduces inflammatory response, inhibits viability, and promotes apoptosis of synovial cells in rat models of rheumatoid arthritis through the MAPK signaling pathway

2019 ◽  
Vol 234 (10) ◽  
pp. 18748-18762 ◽  
Author(s):  
You‐Yu Lan ◽  
You‐Qiang Wang ◽  
Yi Liu
2021 ◽  
Author(s):  
Jieying Wang ◽  
Nanzhen Kuang ◽  
Mao zheng ◽  
Chan Dai ◽  
Huimin Deng ◽  
...  

Abstract Daphnetin(DAP) is extracted from Daphne odora var. marginata and contains coumarin compounds, which have a good anti-inflammatory analgesic effect. In this study, we investigated whether daphnetin can reduce the TNF-α-induced inflammatory response by inhibiting the MAPK signaling pathway in the synovial cells of CIA rats. A model of synovial cells was constructed using CIA rats induced by TNF-α. The expression of inflammatory cytokines in the synovial cells of CIA rats was observed by real-time PCR and ELISA. The expression and nuclear translocation of MAPK signaling pathway proteins were detected by Western blot and immunofluorescence assays. The results show that the mRNA and protein levels of IL-6, TGF-β, MMP-3 and MMP-13 were significantly lower than those in the culture supernatant of the model control group. The synovial cells of CIA rats induced by TNF-α exhibited decreased expression of p-p38, p-ERK1/2 and p-JNK in the nucleus. In conclusion, daphnetin can affect the activation of the MAPK signaling pathway and reduce the expression of inflammatory factors by inhibiting the MAPK signaling pathway, which plays a role in anti-rheumatic inflammation.


2015 ◽  
Vol 66 (2) ◽  
pp. 340-345 ◽  
Author(s):  
Chengcheng Hong ◽  
Chen Shen ◽  
Hongmei Ding ◽  
Shanshan Huang ◽  
Yun Mu ◽  
...  

2021 ◽  
Vol 49 (5) ◽  
pp. 56-62
Author(s):  
Hongtao Chen ◽  
Li Zhang

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 linesinduced 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)、IL-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.


Drug Delivery ◽  
2019 ◽  
Vol 26 (1) ◽  
pp. 1140-1154 ◽  
Author(s):  
Shahira F. El Menshawe ◽  
Mohamed M. Nafady ◽  
Heba M. Aboud ◽  
Rasha M. Kharshoum ◽  
Asmaa Mohammed M. Hussein Elkelawy ◽  
...  

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