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10.1038/aps.2014.98 http://scihub22266oqcxt.onion/10.1038/aps.2014.98 C4571325!4571325 !25500876     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=25500876 &cmd=llinks): Failed to open stream: HTTP request failed! 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Sitagliptin protects rat kidneys from acute ischemia-reperfusion injury via upregulation of GLP-1 and GLP-1 receptors |pdf=|usr=}}{{25500876 }} gab.com Text Sitagliptin protects rat kidneys from acute ischemia-reperfusion injury via upregulation of GLP-1 and GLP-1 receptors JO: Acta Pharmacol Sin http://www.kidney.de/pget.php?&tw=1&pmid=25500876 #FOAvip AIM: Sitagliptin, an oral glucose-lowering agent, has been found to produce cardiovascular protection possibly via anti-inflammatory and anti-atherosclerotic activities of glucagon-like peptide-1 receptor (GLP-1). The aim of this study was to investigate whether sitagliptin protected the kidney function from acute ischemia-reperfusion (IR) injury in rats. METHODS: Adult male SD rats were categorized into 4 groups: sham control, IR injury, IR+sitagliptin (300 mg/kg) and IR+sitagliptin (600 mg/kg). Acute renal IR injury of both kidneys was induced by clamping the renal pedicles for 1 h. The drug was orally administered at 1, 24 and 48 h after acute IR. Blood samples and 24-h urine were collected before and at 72 h after acute IR. Then the rats were sacrificed, and the kidneys were harvested for biochemical and immunohistochemical studies. RESULTS: Acute IR procedure markedly increased serum levels of creatinine and BUN and the ratio of urine protein to creatinine. The kidney injury score, inflammatory biomarkers (MMP-9, TNF-? and NF-?B) levels and CD68+ cells in IR kidneys were considerably increased. The expression of oxidized protein, reactive oxygen species (NOX-1, NOX-2) and apoptosis proteins (Bax, caspase-3, PARP) in IR kidneys was also significantly upregulated. All these pathological changes were suppressed by sitagliptin in a dose-dependent manner. Furthermore, the serum GLP-1 level, and the expression of GLP-1 receptor, anti-oxidant biomarkers (HO-1 and NQO-1 cells, as well as SOD-1, NQO-1 and HO-1 proteins), and angiogenesis markers (SDF-1?+ and CXCR4+ cells) in IR kidneys were significantly increased, and further upregulated by sitagliptin. CONCLUSION: Sitagliptin dose-dependently protects rat kidneys from acute IR injury via upregulation of serum GLP-1 and GLP-1 receptor expression in kidneys. Twit Text FOAVip Sitagliptin protects rat kidneys from acute ischemia-reperfusion injury via upregulation of GLP-1 and GLP-1 receptors ????Acta Pharmacol Sin http://www.kidney.de/pget.php?&tw=1&pmid=25500876 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=25500876 #FOAvip English Wikipedia <ref>{{Cite pmid|25500876 }}</ref> Sitagliptin protects rat kidneys from acute ischemia-reperfusion injury via upregulation of GLP-1 and GLP-1 receptors #MMPMID25500876 Chang MW ; Chen CH ; Chen YC ; Wu YC ; Zhen YY ; Leu S ; Tsai TH ; Ko SF ; Sung PH ; Yang CC ; Chiang HJ ; Chang HW ; Chen YT ; Yip HK Acta Pharmacol Sin 2015[Jan]; 36 (1 ): 119-30 PMID25500876 show ga AIM: Sitagliptin, an oral glucose-lowering agent, has been found to produce cardiovascular protection possibly via anti-inflammatory and anti-atherosclerotic activities of glucagon-like peptide-1 receptor (GLP-1). The aim of this study was to investigate whether sitagliptin protected the kidney function from acute ischemia-reperfusion (IR) injury in rats. METHODS: Adult male SD rats were categorized into 4 groups: sham control, IR injury, IR+sitagliptin (300 mg/kg) and IR+sitagliptin (600 mg/kg). Acute renal IR injury of both kidneys was induced by clamping the renal pedicles for 1 h. The drug was orally administered at 1, 24 and 48 h after acute IR. Blood samples and 24-h urine were collected before and at 72 h after acute IR. Then the rats were sacrificed, and the kidneys were harvested for biochemical and immunohistochemical studies. RESULTS: Acute IR procedure markedly increased serum levels of creatinine and BUN and the ratio of urine protein to creatinine. The kidney injury score, inflammatory biomarkers (MMP-9, TNF-? and NF-?B) levels and CD68+ cells in IR kidneys were considerably increased. The expression of oxidized protein, reactive oxygen species (NOX-1, NOX-2) and apoptosis proteins (Bax, caspase-3, PARP) in IR kidneys was also significantly upregulated. All these pathological changes were suppressed by sitagliptin in a dose-dependent manner. Furthermore, the serum GLP-1 level, and the expression of GLP-1 receptor, anti-oxidant biomarkers (HO-1 and NQO-1 cells, as well as SOD-1, NQO-1 and HO-1 proteins), and angiogenesis markers (SDF-1?+ and CXCR4+ cells) in IR kidneys were significantly increased, and further upregulated by sitagliptin. CONCLUSION: Sitagliptin dose-dependently protects rat kidneys from acute IR injury via upregulation of serum GLP-1 and GLP-1 receptor expression in kidneys. |Animals [MESH] |Glucagon-Like Peptide 1/*metabolism [MESH] |Glucagon-Like Peptide-1 Receptor [MESH] |Kidney/*drug effects/metabolism [MESH] |Male [MESH] |Pyrazines/*pharmacology [MESH] |Rats [MESH] |Rats, Sprague-Dawley [MESH] |Receptors, Glucagon/*metabolism [MESH] |Reperfusion Injury/*drug therapy/metabolism [MESH] |Sitagliptin Phosphate [MESH] |Triazoles/*pharmacology [MESH]Sitagliptin protects rat kidneys from acute ischemia-reperfusion injur(epmc).pdf DeepDyve Pubget Overpricing