Mehrangiz Khanmoradi - Physiology Research Center and Phyiology Department, Faculty of Medicine, Iran University of Medical Sciences, Tehran, Iran
Seyyed Ali Mard - Physiology Research Center (PRC), Research Institute for Infectious Diseases of Digestive System and Department of Physiology, School of Medicine, Jundishapur University of Medical Sciences, Ahvaz, Iran
Nahid Aboutaleb - Physiology Research Center and Phyiology Department, Faculty of Medicine, Iran University of Medical Sciences, Tehran, Iran
Malihe Nobakht - Department of Anatomy, School of Medicine, Iran University of Medical Sciences, Tehran, Iran
Masoud Mahmoudian - Department of Pharmacology, School of Medicine, Iran University of Medical Sciences, Tehran, Iran

Objective(s):Bradykinin is a part of the kinin-kallikreinsystem which is involved in ischemia-reperfusion injury via B۱ and B۲ receptors.Noscapine is a non-competitive antagonist of bradykinin receptors. Noscapine has been reported to to be able to protect some organs against ischemia-reperfusion injury but its effect on renal ischemia-reperfusion injury (RIR) in rats is unknown. Therefore, the present study was designed to evaluate the effect of noscapine on renal ischemia-reperfusion injury in rats. Materials and Methods: Twenty four rats were randomly assigned to four groups; sham, RIR control, pre-and post-treatment with noscapine. To induce RIR injury, ۲۰ days after right nephrectomy, animals underwent a midline laparotomy and the renal artery was clamped for ۴۰ min to induce ischemia, and the clamp was then removed to allow reperfusion for ۴۸ hr. Animals received noscapine or vehicle ۱ hr before RIR or just prior to reperfusion. At the end of the experiment, animals were killed by cardiac exsanguination. Blood samples were collected to assess blood urea nitrogen (BUN) and creatinine. The kidneys were also removed for histopathlogical and western-blot analysis. Results: Noscapine treatment ۱ hr before RIR or just prior to reperfusion protects the renal tissue structure as compared with the control. The expression levels of the studied inflammatory mediators, TNF-α and MCP-۱in pretreated-, and treated-noscapine groups decreased as compared with the control group. The levels of BUN and creatinine in pre-, and post-treated noscapine groups were significantly lower than in control animals. Conclusion: Noscapine protects renal tissue structure and function against RIR through down-regulation of the inflammatory mediators.

BUN, Creatinine, Noscapine, Rat, Renal ischemia-reperfusion injury