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- W4311895961 abstract "Abstract Purpose of the study: Clinical and animal studies had indicated that both inflammation and extracellular matrix metabolism took part in intervertebral disk degeneration. In this study, we investigated the role of adenosine A2a receptor (A2aR) in intervertebral disk and intend to clarify its mechanism. Materials and methods Rat nucleus pulposus (NP) cells were cultured in complete medium, when cells proliferated to the third passage, cells were divided into different groups. Sterile PBS treated for control group, 10ng/ml IL-1β treated NP cells as experimental group, 10ng/ml IL-1β and 10µmol CGS-21680 were added into NP cells, NC siRNA, PKA siRNA and NFκB siRNA stimulated NP cells 24 hours respectively then treated with IL-1β and CGS-21680. Cell proliferation and inflammatory cytokines, collagen, A2aR and their signaling molecules were evaluated. Results IL-1β induced inflammatory cytokine (IL-6 and TNF-α) released and collagen degrading protease (MMP3) overexpression, and A2aR was decreased in NP cells. Protein expression of cAMP, PKA and CREB were decreased, but NFκB was increased. These changes could be reversed by A2aR agonist (CGS-21680). Inflammatory cytokine, MMP3 and NFκB were upregulated in NP cells treated by PKA siRNA, but collagen II was downregulated. Inflammatory cytokine and MMP3 were downregulated in NFκB siRNA treated NP cells, while the expression of collagen II increased. Conclusion Our study hinted that IL-1β induced inflammation and collagen degradation through A2aR, A2aR was a protective receptor. CGS-21680 as the A2aR agonist could alleviate the damage caused by IL-1β. A2aR regulated inflammation and collagen via cAMP-CREB-NFκB axis pathway in NP cells." @default.
- W4311895961 created "2023-01-02" @default.
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- W4311895961 date "2022-12-13" @default.
- W4311895961 modified "2023-10-16" @default.
- W4311895961 title "Adenosine A2a receptor mediate anti-inflammation and collagen protection via cAMP/CREB/NFκB pathway in nucleus pulposus cells" @default.
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- W4311895961 doi "https://doi.org/10.21203/rs.3.rs-2253450/v1" @default.
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