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10.2147/NDT.S140801 http://scihub22266oqcxt.onion/10.2147/NDT.S140801 C5511017!5511017!28744127     free     free     free Deprecated: Implicit conversion from float 213.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 213.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 213.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 213.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 213.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 213.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 247.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Neuropsychiatr+Dis+Treat 2017 ; 13 (ä): 1771-82 Nephropedia Template TP {{tp|p=28744127|t=2017. Necrostatin-1 attenuates early brain injury after subarachnoid hemorrhage in rats by inhibiting necroptosis |pdf=|usr=}}{{28744127}} gab.com Text Necrostatin-1 attenuates early brain injury after subarachnoid hemorrhage in rats by inhibiting necroptosis JO: Neuropsychiatr Dis Treat http://www.kidney.de/pget.php?&tw=1&pmid=28744127 #FOAvip Necroptosis is programmed cell death that has been recently proposed and reported to be involved in several neurologic diseases. However, the role of necroptosis in early brain injury after subarachnoid hemorrhage (SAH) is still unknown. The purpose of this study was to investigate whether necroptosis was involved in SAH-induced early brain injury, and to assess the possible neuroprotective effect of necrostatin-1 using an endovascular perforation rat model of SAH. Our results showed that the expression levels of necroptosis-related proteins including RIP1, RIP3 and MLKL in the basal cortex all increased at 3 hours after SAH (P<0.05) and peaked at 48 hours after SAH (P<0.05). However, they were greatly reduced after treatment with necrostatin-1 (P<0.05). Concurrently, neurologic outcomes were significantly improved after necrostatin-1 treatment (P<0.05). Furthermore, brain edema, blood?brain barrier disruption, necrotic cell death and neuroinflammation were also greatly inhibited after necrostatin-1 treatment. These results indicate that necroptosis is an important mechanism of cell death involved in the early brain injury after experimental SAH. Necrostatin-1 perhaps can serve as a promising neuroprotective agent for SAH treatment. Twit Text FOAVip Necrostatin-1 attenuates early brain injury after subarachnoid hemorrhage in rats by inhibiting necroptosis ????Neuropsychiatr Dis Treat http://www.kidney.de/pget.php?&tw=1&pmid=28744127 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=28744127 #FOAvip English Wikipedia <ref>{{Cite pmid|28744127}}</ref> Necrostatin-1 attenuates early brain injury after subarachnoid hemorrhage in rats by inhibiting necroptosis #MMPMID28744127 Chen F; Su X; Lin Z; Lin Y; Yu L; Cai J; Kang D; Hu L Neuropsychiatr Dis Treat 2017[]; 13 (ä): 1771-82 PMID28744127show ga Necroptosis is programmed cell death that has been recently proposed and reported to be involved in several neurologic diseases. However, the role of necroptosis in early brain injury after subarachnoid hemorrhage (SAH) is still unknown. The purpose of this study was to investigate whether necroptosis was involved in SAH-induced early brain injury, and to assess the possible neuroprotective effect of necrostatin-1 using an endovascular perforation rat model of SAH. Our results showed that the expression levels of necroptosis-related proteins including RIP1, RIP3 and MLKL in the basal cortex all increased at 3 hours after SAH (P<0.05) and peaked at 48 hours after SAH (P<0.05). However, they were greatly reduced after treatment with necrostatin-1 (P<0.05). Concurrently, neurologic outcomes were significantly improved after necrostatin-1 treatment (P<0.05). Furthermore, brain edema, blood?brain barrier disruption, necrotic cell death and neuroinflammation were also greatly inhibited after necrostatin-1 treatment. These results indicate that necroptosis is an important mechanism of cell death involved in the early brain injury after experimental SAH. Necrostatin-1 perhaps can serve as a promising neuroprotective agent for SAH treatment. äNecrostatin-1 attenuates early brain injury after subarachnoid hemorrh(epmc).pdf DeepDyve Pubget Overpricing