Habib Yaribeygi1, Mina Maleki2, Mohammad Taghi Mohammadi3, Thozhukat Sathyapalan4, Tannaz Jamialahmadi5,6, Amirhossein Sahebkar7,8,9. 1. Research Center of Physiology, Semnan University of Medical Sciences, Semnan, Iran. 2. Chronic Kidney Disease Research Center, Shahid Beheshti University of Medical Sciences, Tehran, Iran. 3. Department of Physiology and Biophysics, School of Medicine, Baqiyatallah University of Medical Sciences, Tehran, Iran. 4. Academic Diabetes, Endocrinology and Metabolism, Hull York Medical School, University of Hull, Hull, UK. 5. Department of Food Science and Technology, Quchan Branch, Islamic Azad University, Quchan, Iran. 6. Department of Nutrition, Faculty of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran. 7. Biotechnology Research Center, Pharmaceutical Technology Institute, Mashhad University of Medical Sciences, Mashhad, Iran. sahebkara@mums.ac.ir. 8. Applied Biomedical Research Center, Mashhad University of Medical Sciences, Mashhad, Iran. sahebkara@mums.ac.ir. 9. School of Pharmacy, Mashhad University of Medical Sciences, Mashhad, Iran. sahebkara@mums.ac.ir.
Abstract
BACKGROUND: Oxidative stress has a crucial role in the pathophysiology of cardiac dysfunction in the diabetic milieu. Crocin is a natural compound that acts as an antioxidant which could potentially ameliorate oxidative damages in various tissues. The potential role of crocin in the myocardial tissue is not clear yet. This study was aimed to evaluate the possible antioxidative properties of crocin in the myocardium of diabetic rats. MATERIALS AND METHODS: Male Wistar rats were randomly divided into four groups as normal, normal-treated, diabetic, and diabetic-treated. Diabetes was induced by a single intravenous injection of STZ (40 mg/kg). Two treated groups of animals (diabetic and non-diabetic) were treated with crocin daily for 8 weeks (40 mg/kg/IP). At the end of day 56, animals were sacrificed under deep anesthesia, and blood and tissue samples were collected. After tissue preparation, the level of nitrate, malondialdehyde, and glutathione and the activity of superoxide dismutase and catalase enzymes were measured via standard protocols. In addition, the level of Nox-4 mRNA expression was examined by RT-PCR method. The data were analyzed via one-way ANOVA, and P < 0.05 was considered as a significant difference. RESULTS: Diabetes induces oxidative damages by upregulating the Nox-4 enzyme and increasing nitrate and malondialdehyde levels in the myocardium. Diabetes reduced the superoxide dismutase, catalase, and glutathione activities in the myocardial tissues. Treatment with crocin reversed these changes, reduced Nox-4 mRNA expression, and reduced the nitrate and malondialdehyde content in the myocardium of diabetic rats. CONCLUSION: Diabetes induces oxidative stress in myocardium via the upregulating Nox-4 enzyme, and the treatment with crocin reversed these changes. Thus, crocin could be considered as a novel agent for potentially protecting myocardial tissues against diabetes-induced oxidative damages.
BACKGROUND: Oxidative stress has a crucial role in the pathophysiology of cardiac dysfunction in the diabetic milieu. Crocin is a natural compound that acts as an antioxidant which could potentially ameliorate oxidative damages in various tissues. The potential role of crocin in the myocardial tissue is not clear yet. This study was aimed to evaluate the possible antioxidative properties of crocin in the myocardium of diabetic rats. MATERIALS AND METHODS: Male Wistar rats were randomly divided into four groups as normal, normal-treated, diabetic, and diabetic-treated. Diabetes was induced by a single intravenous injection of STZ (40 mg/kg). Two treated groups of animals (diabetic and non-diabetic) were treated with crocin daily for 8 weeks (40 mg/kg/IP). At the end of day 56, animals were sacrificed under deep anesthesia, and blood and tissue samples were collected. After tissue preparation, the level of nitrate, malondialdehyde, and glutathione and the activity of superoxide dismutase and catalase enzymes were measured via standard protocols. In addition, the level of Nox-4 mRNA expression was examined by RT-PCR method. The data were analyzed via one-way ANOVA, and P < 0.05 was considered as a significant difference. RESULTS: Diabetes induces oxidative damages by upregulating the Nox-4 enzyme and increasing nitrate and malondialdehyde levels in the myocardium. Diabetes reduced the superoxide dismutase, catalase, and glutathione activities in the myocardial tissues. Treatment with crocin reversed these changes, reduced Nox-4 mRNA expression, and reduced the nitrate and malondialdehyde content in the myocardium of diabetic rats. CONCLUSION: Diabetes induces oxidative stress in myocardium via the upregulating Nox-4 enzyme, and the treatment with crocin reversed these changes. Thus, crocin could be considered as a novel agent for potentially protecting myocardial tissues against diabetes-induced oxidative damages.
Authors: Rebecca H Ritchie; Grant R Drummond; Christopher G Sobey; T Michael De Silva; Barbara K Kemp-Harper Journal: Pharmacol Res Date: 2016-12-15 Impact factor: 7.658
Authors: Yosuke Kayama; Uwe Raaz; Ann Jagger; Matti Adam; Isabel N Schellinger; Masaya Sakamoto; Hirofumi Suzuki; Kensuke Toyama; Joshua M Spin; Philip S Tsao Journal: Int J Mol Sci Date: 2015-10-23 Impact factor: 5.923