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10.1172/jci.insight.90777 http://scihub22266oqcxt.onion/10.1172/jci.insight.90777 C5374066!5374066!28405617     free     free     free Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       JCI+Insight ä ; 2 (7): ä Nephropedia Template TP {{tp|p=28405617|t=ä. Inhibition of neuronal ferroptosis protects hemorrhagic brain |pdf=|usr=}}{{28405617}} gab.com Text Inhibition of neuronal ferroptosis protects hemorrhagic brain JO: JCI Insight http://www.kidney.de/pget.php?&tw=1&pmid=28405617 #FOAvip Intracerebral hemorrhage (ICH) causes high mortality and morbidity, but our knowledge of post-ICH neuronal death and related mechanisms is limited. In this study, we first demonstrated that ferroptosis, a newly identified form of cell death, occurs in the collagenase-induced ICH model in mice. We found that administration of ferrostatin-1, a specific inhibitor of ferroptosis, prevented neuronal death and reduced iron deposition induced by hemoglobin in organotypic hippocampal slice cultures (OHSCs). Mice treated with ferrostatin-1 after ICH exhibited marked brain protection and improved neurologic function. Additionally, we found that ferrostatin-1 reduced lipid reactive oxygen species production and attenuated the increased expression level of PTGS2 and its gene product cyclooxygenase-2 ex vivo and in vivo. Moreover, ferrostatin-1 in combination with other inhibitors that target different forms of cell death prevented hemoglobin-induced cell death in OHSCs and human induced pluripotent stem cell?derived neurons better than any inhibitor alone. These results indicate that ferroptosis contributes to neuronal death after ICH, that administration of ferrostatin-1 protects hemorrhagic brain, and that cyclooxygenase-2 could be a biomarker of ferroptosis. The insights gained from this study will advance our knowledge of the post-ICH cell death cascade and be essential for future preclinical studies. Twit Text FOAVip Inhibition of neuronal ferroptosis protects hemorrhagic brain ????JCI Insight http://www.kidney.de/pget.php?&tw=1&pmid=28405617 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=28405617 #FOAvip English Wikipedia <ref>{{Cite pmid|28405617}}</ref> Inhibition of neuronal ferroptosis protects hemorrhagic brain #MMPMID28405617 Li Q; Han X; Lan X; Gao Y; Wan J; Durham F; Cheng T; Yang J; Wang Z; Jiang C; Ying M; Koehler RC; Stockwell BR; Wang J JCI Insight ä[]; 2 (7): ä PMID28405617show ga Intracerebral hemorrhage (ICH) causes high mortality and morbidity, but our knowledge of post-ICH neuronal death and related mechanisms is limited. In this study, we first demonstrated that ferroptosis, a newly identified form of cell death, occurs in the collagenase-induced ICH model in mice. We found that administration of ferrostatin-1, a specific inhibitor of ferroptosis, prevented neuronal death and reduced iron deposition induced by hemoglobin in organotypic hippocampal slice cultures (OHSCs). Mice treated with ferrostatin-1 after ICH exhibited marked brain protection and improved neurologic function. Additionally, we found that ferrostatin-1 reduced lipid reactive oxygen species production and attenuated the increased expression level of PTGS2 and its gene product cyclooxygenase-2 ex vivo and in vivo. Moreover, ferrostatin-1 in combination with other inhibitors that target different forms of cell death prevented hemoglobin-induced cell death in OHSCs and human induced pluripotent stem cell?derived neurons better than any inhibitor alone. These results indicate that ferroptosis contributes to neuronal death after ICH, that administration of ferrostatin-1 protects hemorrhagic brain, and that cyclooxygenase-2 could be a biomarker of ferroptosis. The insights gained from this study will advance our knowledge of the post-ICH cell death cascade and be essential for future preclinical studies. äInhibition of neuronal ferroptosis protects hemorrhagic brain (epmc).pdf DeepDyve Pubget Overpricing