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Article

Diabetes Upregulates Oxidative Stress and Downregulates Cardiac Protection to Exacerbate Myocardial Ischemia/Reperfusion Injury in Rats

1
Department of Surgery, Mackay Memorial Hospital, Taipei 10449, Taiwan
2
Department of Medicine, Mackay Medical College, New Taipei City 25245, Taiwan
3
Mackay Junior College of Medicine, Nursing and Management, New Taipei City 11260, Taiwan
4
Department of Life Science, School of Life Science, National Taiwan Normal University, Taipei 11677, Taiwan
5
Division of Cardiovascular Surgery, National Defense Medical Center, Taipei 11490, Taiwan
6
Division of Cardiovascular Surgery, Heart Center, Cheng Hsin General Hospital, Taipei 11220, Taiwan
*
Authors to whom correspondence should be addressed.
Antioxidants 2020, 9(8), 679; https://doi.org/10.3390/antiox9080679
Received: 17 June 2020 / Revised: 20 July 2020 / Accepted: 22 July 2020 / Published: 29 July 2020
(This article belongs to the Special Issue Free Radicals and Cardiovascular Diseases)
Diabetes exacerbates myocardial ischemia/reperfusion (IR) injury by incompletely understood mechanisms. We explored whether diabetes diminished BAG3/Bcl-2/Nrf-2/HO-1-mediated cardioprotection and overproduced oxidative stress contributing to exaggerated IR injury. Streptozotocin-induced diabetes enhanced hyperglycemia, cardiac NADPH oxidase p22/p67 expression, malondialdehyde amount and leukocyte infiltration, altered the mesenteric expression of 4-HNE, CaSR, p-eNOS and BAG3 and impaired microvascular reactivity to the vasoconstrictor/vasodilator by a wire myography. In response to myocardial IR, diabetes further depressed BAG3/Bcl-2/Nrf-2/HO-1 expression, increased cleaved-caspase 3/poly(ADP-ribose) polymerase (PARP)/TUNEL-mediated apoptosis and exacerbated IR-induced left ventricular dysfunction characterized by further depressed microcirculation, heart rate, left ventricular systolic pressure and peak rate of pressure increase/decrease (±dp/dt) and elevated left ventricular end-diastolic pressure (LVEDP) and Evans blue-2,3,5-triphenyltetrazolium chloride-stained infarct size in diabetic hearts. Our results implicated diabetes exacerbated IR-induced myocardial dysfunction through downregulated BAG3/Bcl-2/Nrf-2/HO-1 expression, increased p22/p67/caspase 3/PARP/apoptosis-mediated oxidative injury and impaired microvascular reactivity. View Full-Text
Keywords: diabetes; myocardial ischemia/reperfusion; oxidative stress; apoptosis diabetes; myocardial ischemia/reperfusion; oxidative stress; apoptosis
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MDPI and ACS Style

Chien, C.-Y.; Wen, T.-J.; Cheng, Y.-H.; Tsai, Y.-T.; Chiang, C.-Y.; Chien, C.-T. Diabetes Upregulates Oxidative Stress and Downregulates Cardiac Protection to Exacerbate Myocardial Ischemia/Reperfusion Injury in Rats. Antioxidants 2020, 9, 679. https://doi.org/10.3390/antiox9080679

AMA Style

Chien C-Y, Wen T-J, Cheng Y-H, Tsai Y-T, Chiang C-Y, Chien C-T. Diabetes Upregulates Oxidative Stress and Downregulates Cardiac Protection to Exacerbate Myocardial Ischemia/Reperfusion Injury in Rats. Antioxidants. 2020; 9(8):679. https://doi.org/10.3390/antiox9080679

Chicago/Turabian Style

Chien, Chen-Yen, Ting-Jui Wen, Yu-Hsiuan Cheng, Yi-Ting Tsai, Chih-Yao Chiang, and Chiang-Ting Chien. 2020. "Diabetes Upregulates Oxidative Stress and Downregulates Cardiac Protection to Exacerbate Myocardial Ischemia/Reperfusion Injury in Rats" Antioxidants 9, no. 8: 679. https://doi.org/10.3390/antiox9080679

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