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10.3892/br.2016.776 http://scihub22266oqcxt.onion/10.3892/br.2016.776 C5103688!5103688 !27882228     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=27882228 &cmd=llinks): Failed to open stream: HTTP request failed! HTTP/1.1 429 Too Many Requests in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 215 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Warning: imagejpeg(C:\Inetpub\vhosts\kidney.de\httpdocs\phplern\27882228 .jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117       Biomed+Rep 2016 ; 5 (5 ): 623-628 Nephropedia Template TP {{tp|p=27882228 |t=2016. Oxymatrine inhibits microglia activation via HSP60-TLR4 signaling |pdf=|usr=}}{{27882228 }} gab.com Text Oxymatrine inhibits microglia activation via HSP60-TLR4 signaling JO: Biomed Rep http://www.kidney.de/pget.php?&tw=1&pmid=27882228 #FOAvip Oxymatrine (OMT) is an alkaloid extracted from Sophora flavescens, which has broad anti-inflammatory, antitumor and immunosuppressant actions. However, the underlying molecular mechanisms have remained elusive. Heat shock protein 60 (HSP60) has recently been shown to have an important role in autoimmune reactions. The present study aimed to investigate whether OMT exerts its anti-inflammatory effects by inhibiting microglial activation and examined the role of HSP60 in this process. Western blot analysis and ELISA showed that OMT decreased the expression and release of HSP60 by LPS-activated BV2 cells. The expression of heat shock factor 1, the transcription factor of HSP60, was also suppressed by OMT. Extracellular HSP60 has been previously indicated to induce microglial apoptosis through the Toll-like receptor (TLR)-4 pathway. Flow cytometric analysis demonstrated that LPS treatment induced apoptosis of BV2 cells, which was inhibited by OMT in parallel with inhibition of LPS-induced expression of TLR-4. Furthermore, OMT was shown to suppress the levels of myeloid differentiation factor (MYD)88, nuclear factor (NF)-?B, caspase-3, inducible nitric oxide synthase, tumor necrosis factor-?, interleukin (IL)-1? and IL-6. In light of these results, it was concluded that OMT may exert its neuroprotective effects via HSP60/TLR-4/MYD88/NF-?B signaling pathways to inhibit microglial activation. OMT may therefore offer substantial therapeutic potential for treating neurodegenerative diseases associated with microglial activation. Twit Text FOAVip Oxymatrine inhibits microglia activation via HSP60-TLR4 signaling ????Biomed Rep http://www.kidney.de/pget.php?&tw=1&pmid=27882228 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=27882228 #FOAvip English Wikipedia <ref>{{Cite pmid|27882228 }}</ref> Oxymatrine inhibits microglia activation via HSP60-TLR4 signaling #MMPMID27882228 Ding F ; Li Y ; Hou X ; Zhang R ; Hu S ; Wang Y Biomed Rep 2016[Nov]; 5 (5 ): 623-628 PMID27882228 show ga Oxymatrine (OMT) is an alkaloid extracted from Sophora flavescens, which has broad anti-inflammatory, antitumor and immunosuppressant actions. However, the underlying molecular mechanisms have remained elusive. Heat shock protein 60 (HSP60) has recently been shown to have an important role in autoimmune reactions. The present study aimed to investigate whether OMT exerts its anti-inflammatory effects by inhibiting microglial activation and examined the role of HSP60 in this process. Western blot analysis and ELISA showed that OMT decreased the expression and release of HSP60 by LPS-activated BV2 cells. The expression of heat shock factor 1, the transcription factor of HSP60, was also suppressed by OMT. Extracellular HSP60 has been previously indicated to induce microglial apoptosis through the Toll-like receptor (TLR)-4 pathway. Flow cytometric analysis demonstrated that LPS treatment induced apoptosis of BV2 cells, which was inhibited by OMT in parallel with inhibition of LPS-induced expression of TLR-4. Furthermore, OMT was shown to suppress the levels of myeloid differentiation factor (MYD)88, nuclear factor (NF)-?B, caspase-3, inducible nitric oxide synthase, tumor necrosis factor-?, interleukin (IL)-1? and IL-6. In light of these results, it was concluded that OMT may exert its neuroprotective effects via HSP60/TLR-4/MYD88/NF-?B signaling pathways to inhibit microglial activation. OMT may therefore offer substantial therapeutic potential for treating neurodegenerative diseases associated with microglial activation. äOxymatrine inhibits microglia activation via HSP60-TLR4 signaling (epmc).pdf DeepDyve Pubget Overpricing