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10.1152/ajprenal.00288.2016 http://scihub22266oqcxt.onion/10.1152/ajprenal.00288.2016 C5504406!5504406 !27358055     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=27358055 &cmd=llinks): Failed to open stream: HTTP request failed! 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The epoxyeicosatrienoic acid analog PVPA ameliorates cyclosporine-induced hypertension and renal injury in rats |pdf=|usr=}}{{27358055 }} gab.com Text The epoxyeicosatrienoic acid analog PVPA ameliorates cyclosporine-induced hypertension and renal injury in rats JO: Am J Physiol Renal Physiol http://www.kidney.de/pget.php?&tw=1&pmid=27358055 #FOAvip The introduction of calcineurin inhibitors (CNI) into clinical practice in the late 1970s transformed organ transplantation and led to significant improvement in acute rejection episodes. However, despite their significant clinical utility, the use of these agents is hampered by the development of hypertension and nephrotoxicity, which ultimately lead to end-stage kidney disease and overt cardiovascular outcomes. There are currently no effective agents to treat or prevent these complications. Importantly, CNI-free immunosuppressive regimens lack the overall efficacy of CNI-based treatments and put patients at risk of allograft rejection. Cytochrome P-450 epoxygenase metabolites of arachidonic acid, epoxyeicosatrienoic acids (EETs), have potent vasodilator and antihypertensive properties in addition to many cytoprotective effects, but their effects on CNI-induced nephrotoxicity have not been explored. Here, we show that PVPA, a novel, orally active analog of 14,15-EET, effectively prevents the development of hypertension and ameliorates kidney injury in cyclosporine-treated rats. PVPA treatment reduced proteinuria and renal dysfunction induced by cyclosporine. PVPA inhibited inflammatory cell infiltration into the kidney and decreased renal fibrosis. PVPA also reduced tubular epithelial cell apoptosis, attenuated the generation of reactive oxygen species, and modulated the unfolded protein response that is associated with endoplasmic reticulum stress. Consistent with the in vivo data, PVPA attenuated cyclosporine-induced apoptosis of NRK-52E cells in vitro. These data indicate that the cytochrome P-450/EET system offers a novel therapeutic strategy to treat or prevent CNI-induced nephrotoxicity. Twit Text FOAVip The epoxyeicosatrienoic acid analog PVPA ameliorates cyclosporine-induced hypertension and renal injury in rats ????Am J Physiol Renal Physiol http://www.kidney.de/pget.php?&tw=1&pmid=27358055 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=27358055 #FOAvip English Wikipedia <ref>{{Cite pmid|27358055 }}</ref> The epoxyeicosatrienoic acid analog PVPA ameliorates cyclosporine-induced hypertension and renal injury in rats #MMPMID27358055 Yeboah MM ; Hye Khan MA ; Chesnik MA ; Sharma A ; Paudyal MP ; Falck JR ; Imig JD Am J Physiol Renal Physiol 2016[Sep]; 311 (3 ): F576-85 PMID27358055 show ga The introduction of calcineurin inhibitors (CNI) into clinical practice in the late 1970s transformed organ transplantation and led to significant improvement in acute rejection episodes. However, despite their significant clinical utility, the use of these agents is hampered by the development of hypertension and nephrotoxicity, which ultimately lead to end-stage kidney disease and overt cardiovascular outcomes. There are currently no effective agents to treat or prevent these complications. Importantly, CNI-free immunosuppressive regimens lack the overall efficacy of CNI-based treatments and put patients at risk of allograft rejection. Cytochrome P-450 epoxygenase metabolites of arachidonic acid, epoxyeicosatrienoic acids (EETs), have potent vasodilator and antihypertensive properties in addition to many cytoprotective effects, but their effects on CNI-induced nephrotoxicity have not been explored. Here, we show that PVPA, a novel, orally active analog of 14,15-EET, effectively prevents the development of hypertension and ameliorates kidney injury in cyclosporine-treated rats. PVPA treatment reduced proteinuria and renal dysfunction induced by cyclosporine. PVPA inhibited inflammatory cell infiltration into the kidney and decreased renal fibrosis. PVPA also reduced tubular epithelial cell apoptosis, attenuated the generation of reactive oxygen species, and modulated the unfolded protein response that is associated with endoplasmic reticulum stress. Consistent with the in vivo data, PVPA attenuated cyclosporine-induced apoptosis of NRK-52E cells in vitro. These data indicate that the cytochrome P-450/EET system offers a novel therapeutic strategy to treat or prevent CNI-induced nephrotoxicity. |Acute Kidney Injury/chemically induced/*drug therapy/pathology [MESH] |Animals [MESH] |Apoptosis/drug effects [MESH] |Arachidonic Acids/pharmacology/*therapeutic use [MESH] |Cyclosporine [MESH] |Endoplasmic Reticulum Stress/drug effects [MESH] |Hypertension/chemically induced/*drug therapy/pathology [MESH] |Immunosuppressive Agents [MESH] |Kidney/*drug effects/pathology [MESH] |Male [MESH] |Oxidative Stress/drug effects [MESH] |Proteinuria/chemically induced/*drug therapy/pathology [MESH] |Rats [MESH]The epoxyeicosatrienoic acid analog PVPA ameliorates cyclosporine-indu(epmc).pdf DeepDyve Pubget Overpricing