Chinese Journal of Tissue Engineering Research ›› 2012, Vol. 16 ›› Issue (31): 5810-5816.doi: 10.3969/j.issn.2095-4344.2012.31.024

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Pyrrolidine dithiocarbamate effects on cell apoptosis in a model of renal ischemia/reperfusion injury

Li Dan, Zhou Hai-yan, Zhang Wei, Xu Yan   

  1. Department of Nephrology, Affiliated Hospital of Qingdao University Medical College, Qingdao 266003, Shandong Province, China
  • Received:2012-01-12 Revised:2012-01-29 Online:2012-07-29 Published:2012-07-29
  • Contact: Xu Yan, Doctor, Chief physician, Department of Nephrology, Affiliated Hospital of Qingdao University Medical College, Qingdao 266003, Shandong Province, China xuyan67@126.com
  • About author:Li Dan★, Studying for master’s degree, Department of Nephrology, Affiliated Hospital of Qingdao University Medical College, Qingdao 266003, Shandong Province, China lidan0823@163.com

Abstract:

BACKGROUND: Renal ischemia/reperfusion (I/R) induces the generation of reactive oxygen species (ROS), which leading to activation of nuclear factor-kappa B (NF-κB). NF-κB regulates production of inducible nitric oxide synthase (iNOS), resulting in increased nitric oxide production and triggering apoptosis.
OBJECTIVE: To evaluate the potential protective effect of pyrrolidine dithiocarbamate effects on NF-κB, iNOS, nitric oxide, caspase-3 and cell apoptotic index in the kidney after I/R.
METHODS: Healthy male Wistar rats were randomly divided into three groups: I/R group: underwent 45 minutes of left renal ischemia and contralateral nephrectomy, established rats renal I/R model. Pyrrolidine dithiocarbamate (PDTC) group: rats were administered PDTC (100 mg/kg intravenous bolus 30 minutes prior to I/R). Sham group: no I/R management.
RESULTS AND CONCLUSION: Compared with sham group, NF-κB, serum creatinine, urea nitrogen, iNOS, nitric oxide, caspase-3 expression and apoptosis were increased (P < 0.05). Compared with I/R group, above-mentioned indices in the PDTC group were improved. These indicate that renal I/R injury could cause renal injury and apoptosis, which was associated with NF-κB induced high expression of nitric oxide. NF-κB inhibitor PDTC obviously protects renal I/R injury.

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