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10.1002/kjm2.12070 http://scihub22266oqcxt.onion/10.1002/kjm2.12070 30977589!ä!30977589 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Kaohsiung+J+Med+Sci 2019 ; 35 (7): 417-424 Nephropedia Template TP {{tp|p=30977589|t=2019. Protective effects of HO-1 pathway on lung injury subsequent to limb ischemia reperfusion |pdf=|usr=}}{{30977589}} gab.com Text Protective effects of HO-1 pathway on lung injury subsequent to limb ischemia reperfusion JO: Kaohsiung J Med Sci http://www.kidney.de/pget.php?&tw=1&pmid=30977589 #FOAvip Limb ischemia reperfusion (LIR) can activate endogenous cytoprotective mechanisms by generating specific proteins against reperfusion injury in remote organs. The present study investigated the roles of heme oxygenase-1 (HO-1) pathway and the molecular mechanisms underlying the regulation of this pathway on lung injury following LIR. LIR was induced by ischemia for 4 hours followed by reperfusion for 6 hours (LIR 6 hours) or 16 hours (LIR 16 hours) in male Sprague-Dawley rats. HO-1 inducer cobalt protoporphyrin (Copp) or HO-1 inhibitor zinc protoporphyrin (Znpp) was intravenously injected 24 hours before ischemia. The animals were randomly divided into nine groups, including normal control, LIR 6 hours, LIR 16 hours, Copp, Copp + LIR 6 hours, Copp + LIR 16 hours, and Znpp, Znpp+ LIR 6 hours, and Znpp + LIR 16 hours groups (each group included four samples). Lung injury was examined through histopathology. Quantitative real-time PCR, immunohistochemistry and Western blot were applied to detect the mRNA and protein levels of HO-1, Nrf2, and Bach1. Our study showed that LIR induced Nrf2 upregulation but Bach1 downregulation to promote HO-1 expression in lung tissues. Activation of HO-1 pathway by Copp potentially enhanced Nrf2 expression but inhibition of the pathway by Znpp promoted Bach1 expression. Inducer of HO-1 pathway, Copp injection improved the lung injury. Nevertheless, Znpp injection aggravated the lung injury following LIR. Our findings suggested that activated HO-1 pathway might exert protective effects on the lung injury following LIR. Twit Text FOAVip Protective effects of HO-1 pathway on lung injury subsequent to limb ischemia reperfusion ????Kaohsiung J Med Sci http://www.kidney.de/pget.php?&tw=1&pmid=30977589 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=30977589 #FOAvip English Wikipedia <ref>{{Cite pmid|30977589}}</ref> Protective effects of HO-1 pathway on lung injury subsequent to limb ischemia reperfusion #MMPMID30977589 Li YY; Liu CY; Liu M; Sun KY Kaohsiung J Med Sci 2019[Jul]; 35 (7): 417-424 PMID30977589show ga Limb ischemia reperfusion (LIR) can activate endogenous cytoprotective mechanisms by generating specific proteins against reperfusion injury in remote organs. The present study investigated the roles of heme oxygenase-1 (HO-1) pathway and the molecular mechanisms underlying the regulation of this pathway on lung injury following LIR. LIR was induced by ischemia for 4 hours followed by reperfusion for 6 hours (LIR 6 hours) or 16 hours (LIR 16 hours) in male Sprague-Dawley rats. HO-1 inducer cobalt protoporphyrin (Copp) or HO-1 inhibitor zinc protoporphyrin (Znpp) was intravenously injected 24 hours before ischemia. The animals were randomly divided into nine groups, including normal control, LIR 6 hours, LIR 16 hours, Copp, Copp + LIR 6 hours, Copp + LIR 16 hours, and Znpp, Znpp+ LIR 6 hours, and Znpp + LIR 16 hours groups (each group included four samples). Lung injury was examined through histopathology. Quantitative real-time PCR, immunohistochemistry and Western blot were applied to detect the mRNA and protein levels of HO-1, Nrf2, and Bach1. Our study showed that LIR induced Nrf2 upregulation but Bach1 downregulation to promote HO-1 expression in lung tissues. Activation of HO-1 pathway by Copp potentially enhanced Nrf2 expression but inhibition of the pathway by Znpp promoted Bach1 expression. Inducer of HO-1 pathway, Copp injection improved the lung injury. Nevertheless, Znpp injection aggravated the lung injury following LIR. Our findings suggested that activated HO-1 pathway might exert protective effects on the lung injury following LIR. |Animals[MESH] |Basic-Leucine Zipper Transcription Factors/genetics/metabolism[MESH] |Enzyme Activators/pharmacology[MESH] |Enzyme Inhibitors/pharmacology[MESH] |Gene Expression Regulation[MESH] |Heme Oxygenase (Decyclizing)/antagonists & inhibitors/*genetics/metabolism[MESH] |Hindlimb/blood supply/drug effects/enzymology[MESH] |Lung[MESH] |Lung Injury/etiology/*genetics/pathology/prevention & control[MESH] |Male[MESH] |NF-E2-Related Factor 2/genetics/metabolism[MESH] |Protoporphyrins/pharmacology[MESH] |RNA, Messenger/genetics/metabolism[MESH] |Rats[MESH] |Rats, Sprague-Dawley[MESH] |Reperfusion Injury/complications/*genetics/pathology/prevention & control[MESH]Protective effects of HO-1 pathway on lung injury subsequent to limb i(epmc).pdf DeepDyve Pubget Overpricing