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10.12659/msm.908616 http://scihub22266oqcxt.onion/10.12659/msm.908616 C5841188!5841188 !29488473     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=29488473 &cmd=llinks): Failed to open stream: HTTP request failed! 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Tetramethylpyrazine Showed Therapeutic Effects on Sepsis-Induced Acute Lung Injury in Rats by Inhibiting Endoplasmic Reticulum Stress Protein Kinase RNA-Like Endoplasmic Reticulum Kinase (PERK) Signaling-Induced Apoptosis of Pulmonary Microvascular Endothelial Cells |pdf=|usr=}}{{29488473 }} gab.com Text Tetramethylpyrazine Showed Therapeutic Effects on Sepsis-Induced Acute Lung Injury in Rats by Inhibiting Endoplasmic Reticulum Stress Protein Kinase RNA-Like Endoplasmic Reticulum Kinase (PERK) Signaling-Induced Apoptosis of Pulmonary Microvascular Endothelial Cells JO: Med Sci Monit http://www.kidney.de/pget.php?&tw=1&pmid=29488473 #FOAvip BACKGROUND Acute lung injury (ALI) is a life-threatening complication of sepsis. Tetramethylpyrazine (TMP) has been used in the clinical treatment of vascular diseases. The aim of this study was to investigate the therapeutic effects and possible involved mechanisms on ALI. MATERIAL AND METHODS Cecal ligation and puncture (CLP) was used to establish a sepsis model in rats. TMP at various dosages were administrated to rats using a intragastric method. Animal survival rate was calculated. The lung functions were evaluated by lung weight/dry weight ratio (W/D), PaO2, dynamic compliance (DC), and airway resistance index (ARI). Pulmonary microvascular endothelial cells (PMVECs) were isolated from lungs harvested from rats with sepsis. TUNEL assay was used to detect apoptosis. Protein expression and phosphorylation levels were assessed by western blotting. RESULTS TMP administration increased the survival rate of septic rats. TMP also decreased W/D and DC, but increased PaO2 and ARI in septic rats. Moreover, PMVECs apoptosis was inhibited in septic rats that received TMP treatment. The expression levels of GRP78, ATF4, caspase-12, active caspase-3, as well as the phosphorylation levels of PERK and eIF2? were suppressed in PMVECs isolated from TMP-treated septic rats. CONCLUSIONS TMP alleviated sepsis-induced ALI by suppressing PMVECs apoptosis via PERK/eIF2?/ATF4/CHOP apoptotic signaling in endoplasmic reticulum stress. Twit Text FOAVip Tetramethylpyrazine Showed Therapeutic Effects on Sepsis-Induced Acute Lung Injury in Rats by Inhibiting Endoplasmic Reticulum Stress Protein Kinase RNA-Like Endoplasmic Reticulum Kinase (PERK) Signaling-Induced Apoptosis of Pulmonary Microvascular Endothelial Cells ????Med Sci Monit http://www.kidney.de/pget.php?&tw=1&pmid=29488473 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=29488473 #FOAvip English Wikipedia <ref>{{Cite pmid|29488473 }}</ref> Tetramethylpyrazine Showed Therapeutic Effects on Sepsis-Induced Acute Lung Injury in Rats by Inhibiting Endoplasmic Reticulum Stress Protein Kinase RNA-Like Endoplasmic Reticulum Kinase (PERK) Signaling-Induced Apoptosis of Pulmonary Microvascular Endothelial Cells #MMPMID29488473 Liu W ; Liu K ; Zhang S ; Shan L ; Tang J Med Sci Monit 2018[Feb]; 24 (ä): 1225-1231 PMID29488473 show ga BACKGROUND Acute lung injury (ALI) is a life-threatening complication of sepsis. Tetramethylpyrazine (TMP) has been used in the clinical treatment of vascular diseases. The aim of this study was to investigate the therapeutic effects and possible involved mechanisms on ALI. MATERIAL AND METHODS Cecal ligation and puncture (CLP) was used to establish a sepsis model in rats. TMP at various dosages were administrated to rats using a intragastric method. Animal survival rate was calculated. The lung functions were evaluated by lung weight/dry weight ratio (W/D), PaO2, dynamic compliance (DC), and airway resistance index (ARI). Pulmonary microvascular endothelial cells (PMVECs) were isolated from lungs harvested from rats with sepsis. TUNEL assay was used to detect apoptosis. Protein expression and phosphorylation levels were assessed by western blotting. RESULTS TMP administration increased the survival rate of septic rats. TMP also decreased W/D and DC, but increased PaO2 and ARI in septic rats. Moreover, PMVECs apoptosis was inhibited in septic rats that received TMP treatment. The expression levels of GRP78, ATF4, caspase-12, active caspase-3, as well as the phosphorylation levels of PERK and eIF2? were suppressed in PMVECs isolated from TMP-treated septic rats. CONCLUSIONS TMP alleviated sepsis-induced ALI by suppressing PMVECs apoptosis via PERK/eIF2?/ATF4/CHOP apoptotic signaling in endoplasmic reticulum stress. |*Apoptosis/drug effects [MESH] |*Endoplasmic Reticulum Stress/drug effects [MESH] |Acute Lung Injury/*drug therapy/etiology/pathology/physiopathology [MESH] |Animals [MESH] |Cell Separation [MESH] |Endothelial Cells/metabolism [MESH] |Kaplan-Meier Estimate [MESH] |Lung/*blood supply [MESH] |Microvessels/*pathology [MESH] |Oxygen/metabolism [MESH] |Pyrazines/administration & dosage/pharmacology/*therapeutic use [MESH] |Rats, Sprague-Dawley [MESH] |Respiratory Function Tests [MESH] |Sepsis/*complications [MESH] |Signal Transduction/drug effects [MESH] |Survival Analysis [MESH]Tetramethylpyrazine Showed Therapeutic Effects on Sepsis-Induced Acute(epmc).pdf DeepDyve Pubget Overpricing