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10.1016/j.chembiol.2017.02.003 http://scihub22266oqcxt.onion/10.1016/j.chembiol.2017.02.003 C5357154!5357154!28238723     free     free     free Warning: imagejpeg(C:\Inetpub\vhosts\kidney.de\httpdocs\phplern\28238723.jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117       Cell+Chem+Biol 2017 ; 24 (3): 281-92 Nephropedia Template TP {{tp|p=28238723|t=2017. NSAIDs are Caspase Inhibitors |pdf=|usr=}}{{28238723}} gab.com Text NSAIDs are Caspase Inhibitors JO: Cell Chem Biol http://www.kidney.de/pget.php?&tw=1&pmid=28238723 #FOAvip Non-steroidal anti-inflammatory drugs (NSAIDs) are among the most commonly used drugs in the world. While the role of NSAIDs as cyclooxygenase (COX) inhibitors is well established, other targets may contribute to anti-inflammation. Here we report caspases as a new pharmacological target for NSAID-family drugs such as ibuprofen, naproxen, and ketorolac at physiologic concentrations both in vitro and in vivo. We characterize caspase activity both in vitro and in cell culture, and combine computational modeling and biophysical analysis to determine the mechanism of action. We observe that inhibition of caspase catalysis reduces cell death and the generation of pro-inflammatory cytokines. Further, NSAID inhibition of caspases is COX-independent, representing a new anti-inflammatory mechanism. This finding expands upon existing NSAID anti-inflammatory behaviors, with implications for patient safety and next-generation drug design. Twit Text FOAVip NSAIDs are Caspase Inhibitors ????Cell Chem Biol http://www.kidney.de/pget.php?&tw=1&pmid=28238723 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=28238723 #FOAvip English Wikipedia <ref>{{Cite pmid|28238723}}</ref> NSAIDs are Caspase Inhibitors #MMPMID28238723 Smith CE; Soti S; Jones TA; Nakagawa A; Xue D; Yin H Cell Chem Biol 2017[Mar]; 24 (3): 281-92 PMID28238723show ga Non-steroidal anti-inflammatory drugs (NSAIDs) are among the most commonly used drugs in the world. While the role of NSAIDs as cyclooxygenase (COX) inhibitors is well established, other targets may contribute to anti-inflammation. Here we report caspases as a new pharmacological target for NSAID-family drugs such as ibuprofen, naproxen, and ketorolac at physiologic concentrations both in vitro and in vivo. We characterize caspase activity both in vitro and in cell culture, and combine computational modeling and biophysical analysis to determine the mechanism of action. We observe that inhibition of caspase catalysis reduces cell death and the generation of pro-inflammatory cytokines. Further, NSAID inhibition of caspases is COX-independent, representing a new anti-inflammatory mechanism. This finding expands upon existing NSAID anti-inflammatory behaviors, with implications for patient safety and next-generation drug design. äNSAIDs are Caspase Inhibitors (epmc).pdf DeepDyve Pubget Overpricing