Gholamali Javedan1, Farzad Shidfar2, Sayed Hossein Davoodi3, Marjan Ajami4, Fazel Gorjipour5, Antoni Sureda6, Seyed Mohammad Nabavi7, Maria Daglia8, Hamidreza Pazoki-Toroudi5. 1. Minimally Invasive Surgery Research Center, Iran University of Medical Sciences, Tehran, Iran. 2. Department of Nutrition, School of Health, Iran University of Medical Sciences, Tehran, Iran. 3. Department of Clinical Nutrition and Dietetic, National Institute and Faculty of Nutrition and Food Technology, Shahid Beheshti University of Medical Sciences, Tehran, Iran. 4. Department of Food and Nutrition Policy and Planning Research, National Nutrition and Food Technology Research Institute, Faculty of Nutrition and Food Technology, Shahid Beheshti University of Medical Sciences, Tehran, Iran. 5. Physiology Research Center and Department of Physiology, Faculty of Medicine, Iran University of Medical Sciences, Tehran, Iran. 6. Research Group on Community Nutrition and Oxidative Stress, University of Balearic Islands, and CIBERobn (Physiopathology of Obesity and Nutrition CB12/03/30038), Palma de Mallorca, Spain. 7. Applied Biotechnology Research Center, Baqiyatallah University of Medical Sciences, Tehran, Iran. 8. Department of Drug Sciences, Medicinal Chemistry and Pharmaceutical Technology Section, University of Pavia, Italy.
Abstract
SCOPE: Conjugated linoleic acids (CLAs) are dietary components with beneficial effects on human health. The aim of this study was to evaluate the potential benefits of CLA pretreatment in a rat model of renal ischemia/reperfusion injury (IRI). METHODS AND RESULTS: Animals were treated with CLAs (200 mg/kg/day) or water for two weeks prior to sham surgery or to surgery to induce IRI. Renal function, oxidative stress, apoptosis, and cell proliferation markers, were evaluated. Moreover, kidney sections were submitted to histological evaluation. IRI induced increased serum creatinine, blood urea nitrogen, fractional sodium excretion, malondialdehyde, Bax, and phosphorylated mammalian target of rapamycin (P-mTOR), and decreased clearance of creatine, superoxide dismutase and catalase activities, and Bax in comparison with control groups. CLA prefeeding restored, at least in part, the above reported markers to normal levels, increased the anti-apoptotic protein, B-cell lymphoma 2 (Bcl-2), and reduce the histological damage. CONCLUSION: The results suggest that the decreased renal tissue damage and improved renal function and oxidative stress, in rats pretreated with CLAs before renal IRI induction, could be associated with downregulation of Bax and P-mTOR, and upregulation of Bcl-2. CLAs pretreatment resulted to protect against IRI through the regulation of signaling pathways involved in apoptosis.
SCOPE: Conjugated linoleic acids (CLAs) are dietary components with beneficial effects on human health. The aim of this study was to evaluate the potential benefits of CLA pretreatment in a rat model of renal ischemia/reperfusion injury (IRI). METHODS AND RESULTS: Animals were treated with CLAs (200 mg/kg/day) or water for two weeks prior to sham surgery or to surgery to induce IRI. Renal function, oxidative stress, apoptosis, and cell proliferation markers, were evaluated. Moreover, kidney sections were submitted to histological evaluation. IRI induced increased serum creatinine, blood ureanitrogen, fractional sodium excretion, malondialdehyde, Bax, and phosphorylated mammalian target of rapamycin (P-mTOR), and decreased clearance of creatine, superoxide dismutase and catalase activities, and Bax in comparison with control groups. CLA prefeeding restored, at least in part, the above reported markers to normal levels, increased the anti-apoptotic protein, B-cell lymphoma 2 (Bcl-2), and reduce the histological damage. CONCLUSION: The results suggest that the decreased renal tissue damage and improved renal function and oxidative stress, in rats pretreated with CLAs before renal IRI induction, could be associated with downregulation of Bax and P-mTOR, and upregulation of Bcl-2. CLAs pretreatment resulted to protect against IRI through the regulation of signaling pathways involved in apoptosis.