title: Notoginsenoside R1 attenuates renal ischemia-reperfusion injury in rats.
abstract: Ischemia-reperfusion (I/R) injury of the kidney is a complex pathophysiological process and a major cause of acute renal failure. It has been shown that I/R injury is related to inflammatory responses and activation of apoptotic pathways. Inhibition of certain elements of inflammatory responses and apoptotic pathway seemed to ameliorate renal I/R injury. As an effective element of Panax notoginseng, NR1 has antioxidant, anti-inflammatory, antiapoptotic, and immune-stimulatory activities. Therefore, we speculate that NR1 can attenuate renal I/R injury. Ischemia-reperfusion injury was induced by renal pedicle ligation followed by reperfusion along with a contralateral nephrectomy. Male Sprague-Dawley rats were randomized to four groups: sham group, I/R control group, NR1-1 group (rats treated with NR1, 20 mg.kg.d) and NR1-2 group (rats treated with NR1, 40 mg.kg.d). All animals were killed 72 h after I/R induction. Blood and renal tissues were collected. Renal dysfunction was observed by the level of serum creatinine and histological evaluation. Apoptosis and inflammatory response in the tissue of kidney were detected mainly with molecular biological methods. NR1 attenuated I/R-induced renal dysfunction as indicated by the level of serum creatinine and histological evaluation. It prevented the I/R-induced increases in the levels of proinflammatory cytokine TNF-alpha, myeloperoxidase activity, phosphorylation of p38, and activation of nuclear factor kappaB with cell apoptosis in the kidney and enhanced expression of antiapoptosis cytokine bcl-2. Treatment with NR1 improves renal function after I/R associated with a significant reduction in cell apoptosis and inflammatory responses, which may be related to p38 and nuclear factor kappaB inhibition.
authors.affiliation: Department of Burn Surgery, Changhai Hospital, Second Military Medical University, Shanghai, People's Republic of China.
authors.forename: Wen-Jun
authors.initials: WJ
authors.lastname: Liu
authors.forename: Hong-Tai
authors.initials: HT
authors.lastname: Tang
authors.forename: Yi-Tao
authors.initials: YT
authors.lastname: Jia
authors.forename: Bing
authors.initials: B
authors.lastname: Ma
authors.forename: Jin-Feng
authors.initials: JF
authors.lastname: Fu
authors.forename: Yu
authors.initials: Y
authors.lastname: Wang
authors.forename: Kai-Yang
authors.initials: KY
authors.lastname: Lv
authors.forename: Zhao-Fan
authors.initials: ZF
authors.lastname: Xia
mesh_terms: D000818:Animals; D017209:Apoptosis / Q000187:drug effects; D003404:Creatinine / Q000097:blood; D016207:Cytokines / Q000097:blood; D004353:Drug Evaluation, Preclinical; D004365:Drugs, Chinese Herbal / Q000494:pharmacology / Q000627:therapeutic use*; D019254:Genes, bcl-2; D036145:Ginsenosides / Q000494:pharmacology / Q000627:therapeutic use*; D007668:Kidney / Q000098:blood supply* / Q000473:pathology / Q000503:physiopathology; D008297:Male; D016328:NF-kappa B / Q000378:metabolism; D009504:Neutrophils / Q000201:enzymology; D009195:Peroxidase / Q000032:analysis; D019253:Proto-Oncogene Proteins c-bcl-2 / Q000096:biosynthesis; D011897:Random Allocation; D051381:Rats; D017207:Rats, Sprague-Dawley; D012079:Renal Circulation / Q000187:drug effects; D015427:Reperfusion Injury / Q000517:prevention & control*; D048051:p38 Mitogen-Activated Protein Kinases / Q000378:metabolism
chemical_list: D016207:Cytokines; D004365:Drugs, Chinese Herbal; D036145:Ginsenosides; D016328:NF-kappa B; D019253:Proto-Oncogene Proteins c-bcl-2; D003404:Creatinine; D009195:Peroxidase; D048051:p38 Mitogen-Activated Protein Kinases; C072936:notoginsenoside R1