Pterostilbene protects against myocardial ischemia/reperfusion injury via suppressing oxidative/nitrative stress and inflammatory response |
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| Institution: | 1. Department of Intensive Care Unit, First Affiliated Hospital of Xinjiang Medical University, Urumqi 830054, China;2. Department of Neurosurgery, Second Affiliated Hospital of Anhui Medical University, Hefei 230000, China;3. Cardiac Center, First Affiliated Hospital of Xinjiang Medical University, Urumqi 830054, China;4. Institute of Clinical Medicine Research, First Affiliated Hospital of Xinjiang Medical University, Urumqi 830054, China;1. Department of Physiology and Pharmacology, China Pharmaceutical University, Tongjiaxiang 24, Nanjing 210009, China;2. Department of Pharmacology of Chinese Materia Medica, China Pharmaceutical University, Nanjing 210009, China;1. Department of Pathology, School of Basic Medical Sciences, Capital Medical University, Beijing, China;2. Department of Physiology and Physiopathology, School of Basic Medical Sciences, Capital Medical University, Beijing, China;3. Department of Vascular Surgery, Peking University First Hospital, Beijing, China |
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| Abstract: | Recent studies have shown that pterostilbene (Pte) confers protection against myocardial ischemia/reperfusion injury. The oxidative/nitrative stress and inflammation induce injury after myocardial ischemia/reperfusion. The present study was designed to evaluate whether treatment with Pte attenuates oxidative/nitrative stress and inflammation in myocardial ischemia/reperfusion (MI/R). Rats were subjected to 30 min of myocardial ischemia and 3 h of reperfusion, and the rats were administered with vehicle or Pte. The results showed that Pte (10 mg/kg) dramatically improved cardiac function and reduced myocardial infarction and myocardial apoptosis following MI/R. As an indicator of oxidative/nitrative stress, myocardial ONOO− content was markedly reduced after Pte treatment. And, Pte led to a dramatic decrease in superoxide generation and malondialdehyde (MDA) content and a dramatic increase in superoxide dismutase (SOD) activity. In addition, Pte treatment significantly reduced p38 MAPK activation and the expression of iNOS and gp91phox and increased phosphorylated eNOS expression. Pte treatment dramatically decreased myocardial TNF-α, and IL-1β levels and myeloperoxidase (MPO) activity. Furthermore, ONOO− suppression by either Pte or uric acid (UA), an ONOO− scavenger, reduced myocardial injury. In conclusion, Pte exerts a protective effect against MI/R injury by suppressing oxidative/nitrative stress. These results provide evidence that Pte might be a therapeutic approach for the treatment of MI/R injury. |
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