Nephroprotective Effects of Polydatin against Ischemia/Reperfusion Injury: A Role for the PI3K/Akt Signal Pathway

Autor: Hongbao Liu, Chen Huang, Xiao-Wei Liu, Qiu-Hong Meng, Jian-Bo Wang
Rok vydání: 2015
Předmět:
Male
Aging
Interleukin-1beta
Nitric Oxide Synthase Type II
Pharmacology
Kidney
medicine.disease_cause
Biochemistry
Antioxidants
Mice
Phosphatidylinositol 3-Kinases
chemistry.chemical_compound
Glucosides
Stilbenes
chemistry.chemical_classification
Mice
Inbred BALB C
biology
lcsh:Cytology
Glutathione peroxidase
General Medicine
Up-Regulation
Nitric oxide synthase
medicine.anatomical_structure
Reperfusion Injury
Oxidoreductases
Signal Transduction
Research Article
Article Subject
Protective Agents
Nitric oxide
medicine
Animals
lcsh:QH573-671
PI3K/AKT/mTOR pathway
Renal ischemia
Tumor Necrosis Factor-alpha
business.industry
Cell Biology
medicine.disease
Disease Models
Animal
Oxidative Stress
chemistry
Cyclooxygenase 2
biology.protein
business
Proto-Oncogene Proteins c-akt
Reperfusion injury
Oxidative stress
Zdroj: Oxidative Medicine and Cellular Longevity
Oxidative Medicine and Cellular Longevity, Vol 2015 (2015)
ISSN: 1942-0994
1942-0900
DOI: 10.1155/2015/362158
Popis: Oxidative stress and inflammation are involved in the pathogenesis in renal ischemia/reperfusion (I/R) injury. It has been demonstrated that polydatin processed the antioxidative, anti-inflammatory, and nephroprotective properties. However, whether it has beneficial effects and the possible mechanisms on renal I/R injury remain unclear. In our present study I/R models were simulated bothin vitroandin vivo. Compared with vehicle control, the administration of polydatin significantly improved the renal function, accelerated the mitogenic response and reduced cell apoptosis in renal I/R injury models, strongly suppressed the I/R-induced upregulation of the expression of tumor necrosis factor-α, interleukin-1β, cyclooxygenase-2, inducible nitric oxide synthase, prostaglandin E-2, and nitric oxide levels, and dramatically decreased contents of malondialdehyde, but it increased the activity of superoxide dismutase, glutathione transferase, glutathione peroxidase and catalase, and the level of glutathione. Further investigation showed that polydatin upregulated the phosphorylation of Akt in kidneys of I/R injury dose-dependently. However, all beneficial effects of polydatin mentioned above were counteracted when we inhibited PI3K/Akt pathway with its specific inhibitor, wortmannin. Taken together, the present findings provide the first evidence demonstrating that PD exhibited prominent nephroprotective effects against renal I/R injury by antioxidative stress and inflammation through PI3-K/Akt-dependent molecular mechanisms.
Databáze: OpenAIRE
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