@article{ chander_protective_2006,
  title = {Protective {Effect} of {Nitric} {Oxide} {Pathway} in {Resveratrol} {Renal} {Ischemia}-{Reperfusion} {Injury} in {Rats}},
  volume = {37},
  issn = {0188-4409},
  url = {http://www.sciencedirect.com/science/article/pii/S0188440905002419},
  doi = {10.1016/j.arcmed.2005.05.018},
  abstract = {Background
Nitric oxide (NO), synthesized from L-arginine by the enzyme nitric oxide synthase (NOS), seems to play an ambiguous role during tissue ischemia-reperfusion (I/R) injury. This study was designed to investigate the effects of resveratrol, a polyphenolic phytoalexin, in renal ischemia reperfusion (RIR) injury in rats.
Methods
Forty-eight rats were randomized into six groups. Group 1: sham operated (C); group 2: right nephrectomy (UNI); group 3: UNI + 45 min of ischemia and 24 h of reperfusion in the contralateral kidney; group 4: UNI + RIR + L-NAME (10 mg/kg, i.p.); group 5: UNI + RIR + resveratrol (5 mg/kg, p.o.); group 6: UNI + RIR + resveratrol + L-NAME. At the end of the reperfusion period, rats were sacrificed. Thiobarbituric acid reactive substances (TBARS), reduced glutathione (GSH) levels, catalase (CAT), and superoxide dismutase (SOD) activities were determined in renal tissue. Serum creatinine and blood urea nitrogen (BUN) were measured for the evaluation of renal function. Tissue and urine nitrite levels were measured to assess total nitric oxide levels.
Results
Ischemic control animals demonstrated severe deterioration of renal function, altered renal morphology, reduced total nitric oxide levels and a marked renal oxidative stress.
Conclusions
Pretreatment of animals with resveratrol markedly attenuated renal dysfunction, morphological alterations, improved nitric oxide levels, reduced elevated TBARS levels and restored the depleted renal antioxidant enzymes, However, treatment with L-NAME attenuated this protection afforded by resveratrol indicating that resveratrol exerts its protective effect through NO release.},
  number = {1},
  urldate = {2015-05-14TZ},
  journal = {Archives of Medical Research},
  author = {Chander, Vikas and Chopra, Kanwaljit},
  year = {2006},
  keywords = {Ischemia-reperfusion, Nitric Oxide, Oxidative Stress, resveratrol},
  pages = {19--26}
}

{"_id":"yRPXL7iZjvLHF2Lox","bibbaseid":"chander-chopra-protectiveeffectofnitricoxidepathwayinresveratrolrenalischemiareperfusioninjuryinrats-2006","downloads":0,"creationDate":"2015-06-15T14:51:24.250Z","title":"Protective Effect of Nitric Oxide Pathway in Resveratrol Renal Ischemia-Reperfusion Injury in Rats","author_short":["Chander, V.","Chopra, K."],"year":2006,"bibtype":"article","biburl":"http://bibbase.org/zotero/yishin0819","bibdata":{"abstract":"Background Nitric oxide (NO), synthesized from L-arginine by the enzyme nitric oxide synthase (NOS), seems to play an ambiguous role during tissue ischemia-reperfusion (I/R) injury. This study was designed to investigate the effects of resveratrol, a polyphenolic phytoalexin, in renal ischemia reperfusion (RIR) injury in rats. Methods Forty-eight rats were randomized into six groups. Group 1: sham operated (C); group 2: right nephrectomy (UNI); group 3: UNI + 45 min of ischemia and 24 h of reperfusion in the contralateral kidney; group 4: UNI + RIR + L-NAME (10 mg/kg, i.p.); group 5: UNI + RIR + resveratrol (5 mg/kg, p.o.); group 6: UNI + RIR + resveratrol + L-NAME. At the end of the reperfusion period, rats were sacrificed. Thiobarbituric acid reactive substances (TBARS), reduced glutathione (GSH) levels, catalase (CAT), and superoxide dismutase (SOD) activities were determined in renal tissue. Serum creatinine and blood urea nitrogen (BUN) were measured for the evaluation of renal function. Tissue and urine nitrite levels were measured to assess total nitric oxide levels. Results Ischemic control animals demonstrated severe deterioration of renal function, altered renal morphology, reduced total nitric oxide levels and a marked renal oxidative stress. Conclusions Pretreatment of animals with resveratrol markedly attenuated renal dysfunction, morphological alterations, improved nitric oxide levels, reduced elevated TBARS levels and restored the depleted renal antioxidant enzymes, However, treatment with L-NAME attenuated this protection afforded by resveratrol indicating that resveratrol exerts its protective effect through NO release.","author":["Chander, Vikas","Chopra, Kanwaljit"],"author_short":["Chander, V.","Chopra, K."],"bibtex":"@article{ chander_protective_2006,\n title = {Protective {Effect} of {Nitric} {Oxide} {Pathway} in {Resveratrol} {Renal} {Ischemia}-{Reperfusion} {Injury} in {Rats}},\n volume = {37},\n issn = {0188-4409},\n url = {http://www.sciencedirect.com/science/article/pii/S0188440905002419},\n doi = {10.1016/j.arcmed.2005.05.018},\n abstract = {Background\nNitric oxide (NO), synthesized from L-arginine by the enzyme nitric oxide synthase (NOS), seems to play an ambiguous role during tissue ischemia-reperfusion (I/R) injury. This study was designed to investigate the effects of resveratrol, a polyphenolic phytoalexin, in renal ischemia reperfusion (RIR) injury in rats.\nMethods\nForty-eight rats were randomized into six groups. Group 1: sham operated (C); group 2: right nephrectomy (UNI); group 3: UNI + 45 min of ischemia and 24 h of reperfusion in the contralateral kidney; group 4: UNI + RIR + L-NAME (10 mg/kg, i.p.); group 5: UNI + RIR + resveratrol (5 mg/kg, p.o.); group 6: UNI + RIR + resveratrol + L-NAME. At the end of the reperfusion period, rats were sacrificed. Thiobarbituric acid reactive substances (TBARS), reduced glutathione (GSH) levels, catalase (CAT), and superoxide dismutase (SOD) activities were determined in renal tissue. Serum creatinine and blood urea nitrogen (BUN) were measured for the evaluation of renal function. Tissue and urine nitrite levels were measured to assess total nitric oxide levels.\nResults\nIschemic control animals demonstrated severe deterioration of renal function, altered renal morphology, reduced total nitric oxide levels and a marked renal oxidative stress.\nConclusions\nPretreatment of animals with resveratrol markedly attenuated renal dysfunction, morphological alterations, improved nitric oxide levels, reduced elevated TBARS levels and restored the depleted renal antioxidant enzymes, However, treatment with L-NAME attenuated this protection afforded by resveratrol indicating that resveratrol exerts its protective effect through NO release.},\n number = {1},\n urldate = {2015-05-14TZ},\n journal = {Archives of Medical Research},\n author = {Chander, Vikas and Chopra, Kanwaljit},\n year = {2006},\n keywords = {Ischemia-reperfusion, Nitric Oxide, Oxidative Stress, resveratrol},\n pages = {19--26}\n}","bibtype":"article","doi":"10.1016/j.arcmed.2005.05.018","id":"chander_protective_2006","issn":"0188-4409","journal":"Archives of Medical Research","key":"chander_protective_2006","keywords":"Ischemia-reperfusion, Nitric Oxide, Oxidative Stress, resveratrol","number":"1","pages":"19--26","title":"Protective Effect of Nitric Oxide Pathway in Resveratrol Renal Ischemia-Reperfusion Injury in Rats","type":"article","url":"http://www.sciencedirect.com/science/article/pii/S0188440905002419","urldate":"2015-05-14TZ","volume":"37","year":"2006","bibbaseid":"chander-chopra-protectiveeffectofnitricoxidepathwayinresveratrolrenalischemiareperfusioninjuryinrats-2006","role":"author","urls":{"Paper":"http://www.sciencedirect.com/science/article/pii/S0188440905002419"},"keyword":["Ischemia-reperfusion","Nitric Oxide","Oxidative Stress","resveratrol"],"downloads":0},"search_terms":["protective","effect","nitric","oxide","pathway","resveratrol","renal","ischemia","reperfusion","injury","rats","chander","chopra"],"keywords":["ischemia-reperfusion","nitric oxide","oxidative stress","resveratrol"],"authorIDs":[],"dataSources":["5a9x8gDFLeNBehhXX"]}