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http://scihub22266oqcxt.onion/ C5375994!5375994 !28386329     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=28386329 &cmd=llinks): Failed to open stream: HTTP request failed! 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Inhibiting endoplasmic reticulum stress by lithium chloride contributes to the integrity of blood-spinal cord barrier and functional recovery after spinal cord injury |pdf=|usr=}}{{28386329 }} gab.com Text Inhibiting endoplasmic reticulum stress by lithium chloride contributes to the integrity of blood-spinal cord barrier and functional recovery after spinal cord injury JO: Am J Transl Res http://www.kidney.de/pget.php?&tw=1&pmid=28386329 #FOAvip Endoplasmic reticulum (ER) stress play important roles in the spinal cord injury (SCI), which including blood-spinal cord barrier (BSCB) disruption. Lithium chloride (LiCl) is a clinical drug for bipolar mood disorders and contributes to neuroprotection. This study aims to investigate the effects of LiCl on BSCB disruption and the ER stress pathway induced by spinal cord injury. We examined the integrity of the BSCB with Evans Blue dye and macrophages extravasation, measured the microvessels loss, the junction proteins degeneration, the activation ER stress, and the locomotor function recovery. Our data indicated that LiCl treatment could attenuates BSCB disruption and improved the recovery of functional locomotion in rats SCI model, reduced the structure damage and number loss of microvessels, increased the expressions of junction proteins, including p120, ?-catenin, occludin, and claudin-5, via reversed the upregulated ER stress associated proteins. In addition, LiCl significantly inhibited the increase of ER stress markers and prevents loss of junction proteins in thapsigargin (TG)-treated human brain microvascular endothelial cells (HBMEC). These findings suggest that LiCl treatment alleviates BSCB disruption and promote the neurological function recovery after SCI, partly through inhibiting the activation of ER stress. Twit Text FOAVip Inhibiting endoplasmic reticulum stress by lithium chloride contributes to the integrity of blood-spinal cord barrier and functional recovery after spinal cord injury ????Am J Transl Res http://www.kidney.de/pget.php?&tw=1&pmid=28386329 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=28386329 #FOAvip English Wikipedia <ref>{{Cite pmid|28386329 }}</ref> Inhibiting endoplasmic reticulum stress by lithium chloride contributes to the integrity of blood-spinal cord barrier and functional recovery after spinal cord injury #MMPMID28386329 He Z ; Zhou Y ; Wang Q ; Li J ; Zheng Z ; Chen J ; Zhang H ; Wang Z ; Xu H ; Xiao J Am J Transl Res 2017[]; 9 (3 ): 1012-1024 PMID28386329 show ga Endoplasmic reticulum (ER) stress play important roles in the spinal cord injury (SCI), which including blood-spinal cord barrier (BSCB) disruption. Lithium chloride (LiCl) is a clinical drug for bipolar mood disorders and contributes to neuroprotection. This study aims to investigate the effects of LiCl on BSCB disruption and the ER stress pathway induced by spinal cord injury. We examined the integrity of the BSCB with Evans Blue dye and macrophages extravasation, measured the microvessels loss, the junction proteins degeneration, the activation ER stress, and the locomotor function recovery. Our data indicated that LiCl treatment could attenuates BSCB disruption and improved the recovery of functional locomotion in rats SCI model, reduced the structure damage and number loss of microvessels, increased the expressions of junction proteins, including p120, ?-catenin, occludin, and claudin-5, via reversed the upregulated ER stress associated proteins. In addition, LiCl significantly inhibited the increase of ER stress markers and prevents loss of junction proteins in thapsigargin (TG)-treated human brain microvascular endothelial cells (HBMEC). These findings suggest that LiCl treatment alleviates BSCB disruption and promote the neurological function recovery after SCI, partly through inhibiting the activation of ER stress. äInhibiting endoplasmic reticulum stress by lithium chloride contribute(epmc).pdf DeepDyve Pubget Overpricing