Skip to main content
Top
Published in: BMC Cardiovascular Disorders 1/2021

Open Access 01-12-2021 | Myocardial Infarction | Research article

The disappearance of IPO in myocardium of diabetes mellitus rats is associated with the increase of succinate dehydrogenase-flavin protein

Authors: Mengyuan Deng, Wei Chen, Haiying Wang, Yan Wang, Wenjing Zhou, Tian Yu

Published in: BMC Cardiovascular Disorders | Issue 1/2021

Login to get access

Abstract

Background

The aim of the present study was to investigate whether the disappearance of ischemic post-processing (IPO) in the myocardium of diabetes mellitus (DM) is associated with the increase of succinate dehydrogenase-flavin protein (SDHA).

Methods

A total of 50 Sprague Dawley rats, weighing 300–400 g, were divided into 5 groups according to the random number table method, each with 10 rats. After DM rats were fed a high-fat and -sugar diet for 4 weeks, they were injected with Streptozotocin to establish the diabetic rat model. Normal rats were fed the same regular diet for the same number of weeks. Next, the above rats were taken to establish a cardiopulmonary bypass (CPB) model. Intraperitoneal glucose tolerance test (IPGTT) and oral glucose tolerance test (OGTT) were used to detect whether the DM rat model was established successfully. Taking blood from the femoral artery to collect the blood-gas analysis indicators, and judged whether the CPB model is established. After perfusion was performed according to the experimental strategy, the area of myocardial infarction (MI), and serum creatine kinase isoenzyme (CK-MB) and cardiac troponin (CTnI) levels were measured. Finally, the relative mRNA and protein expression of SDHA was detected.

Results

The OGTT and IPGTT suggested that the DM rat model was successfully established. The arterial blood gas analysis indicated that the CPB model was successfully established. As compared with the N group, the heart function of the IR group was significantly reduced, the levels of myocardial enzyme markers, the area of MI, as well as the relative mRNA and protein expression of SDHA, were all increased. As compared with the IR group, the CK-MB and CTnI levels in the IPO group, the MI area, relative mRNA and protein expression of SDHA decreased. As compared with the IPO group, the myocardial enzyme content in the DM + IPO group, the MI area and the relative mRNA and protein expression of SDHA increased. As compared with the DM + IPO group, in the DM + IPO + dme group, the myocardial enzyme content, area of MI and relative mRNA and protein expression were all decreased.

Conclusion

IPO can inhibit the expression of SDHA, reduce MIRI and exert a cardioprotective effect in the normal rats. However, the protective effect of IPO disappears in the diabetic rats. The inhibitor dme combined with IPO can increase the expression of SDHA and restore the protective effect of IPO in DM myocardia.
Appendix
Available only for authorised users
Literature
1.
go back to reference Houstis N, Rosen ED, Lander ES. Reactive oxygen species have a causal role in multiple forms of insulin resistance. Nature. 2006;440(7086):944–8.PubMedCrossRef Houstis N, Rosen ED, Lander ES. Reactive oxygen species have a causal role in multiple forms of insulin resistance. Nature. 2006;440(7086):944–8.PubMedCrossRef
2.
3.
go back to reference Naryzhnaya NV, Maslov LN, Oeltgen PR. Pharmacology of mitochondrial permeability transition pore inhibitors. Drug Dev Res. 2019;80(8):1013–30.PubMedCrossRef Naryzhnaya NV, Maslov LN, Oeltgen PR. Pharmacology of mitochondrial permeability transition pore inhibitors. Drug Dev Res. 2019;80(8):1013–30.PubMedCrossRef
4.
go back to reference Loboda A, Damulewicz M, Pyza E, Jozkowicz A, Dulak J. Role of Nrf2/HO-1 system in development, oxidative stress response and diseases: an evolutionarily conserved mechanism. Cell Mol Life Sci. 2016;73(17):3221–47.PubMedPubMedCentralCrossRef Loboda A, Damulewicz M, Pyza E, Jozkowicz A, Dulak J. Role of Nrf2/HO-1 system in development, oxidative stress response and diseases: an evolutionarily conserved mechanism. Cell Mol Life Sci. 2016;73(17):3221–47.PubMedPubMedCentralCrossRef
5.
go back to reference Jia Z, Lian W, Shi H, et al. Ischemic postconditioning protects against intestinal ischemia/reperfusion injury via the HIF-1α/miR-21 Axis. Sci Rep. 2017;7(1):16190.PubMedPubMedCentralCrossRef Jia Z, Lian W, Shi H, et al. Ischemic postconditioning protects against intestinal ischemia/reperfusion injury via the HIF-1α/miR-21 Axis. Sci Rep. 2017;7(1):16190.PubMedPubMedCentralCrossRef
6.
go back to reference Baranyai T, Nagy CT, Koncsos G, et al. Acute hyperglycemia abolishes cardioprotection by remote ischemic perconditioning. Cardiovasc Diabetol. 2015;14:151.PubMedPubMedCentralCrossRef Baranyai T, Nagy CT, Koncsos G, et al. Acute hyperglycemia abolishes cardioprotection by remote ischemic perconditioning. Cardiovasc Diabetol. 2015;14:151.PubMedPubMedCentralCrossRef
7.
go back to reference Han Z, Cao J, Song D, et al. Autophagy is involved in the cardioprotection effect of remote limb ischemic postconditioning on myocardial ischemia/reperfusion injury in normal mice, but not diabetic mice. PLoS ONE. 2014;9(1):e86838.PubMedPubMedCentralCrossRef Han Z, Cao J, Song D, et al. Autophagy is involved in the cardioprotection effect of remote limb ischemic postconditioning on myocardial ischemia/reperfusion injury in normal mice, but not diabetic mice. PLoS ONE. 2014;9(1):e86838.PubMedPubMedCentralCrossRef
8.
go back to reference Chen Y, Zhao L, Jiang S, et al. Cystathionine γ-lyase is involved in the renoprotective effect of brief and repeated ischemic postconditioning after renal ischemia/reperfusion injury in diabetes mellitus. Transplant Proc. 2018;50(5):1549–57.PubMedCrossRef Chen Y, Zhao L, Jiang S, et al. Cystathionine γ-lyase is involved in the renoprotective effect of brief and repeated ischemic postconditioning after renal ischemia/reperfusion injury in diabetes mellitus. Transplant Proc. 2018;50(5):1549–57.PubMedCrossRef
9.
go back to reference Hausenloy DJ, Yellon DM. New directions for protecting the heart against ischaemia-reperfusion injury: targeting the Reperfusion Injury Salvage Kinase (RISK)-pathway. Cardiovasc Res. 2004;61(3):448–60.PubMedCrossRef Hausenloy DJ, Yellon DM. New directions for protecting the heart against ischaemia-reperfusion injury: targeting the Reperfusion Injury Salvage Kinase (RISK)-pathway. Cardiovasc Res. 2004;61(3):448–60.PubMedCrossRef
10.
go back to reference Zhang M, Sun D, Li S, et al. Lin28a protects against cardiac ischaemia/reperfusion injury in diabetic mice through the insulin-PI3K-mTOR pathway. J Cell Mol Med. 2015;19(6):1174–82.PubMedPubMedCentralCrossRef Zhang M, Sun D, Li S, et al. Lin28a protects against cardiac ischaemia/reperfusion injury in diabetic mice through the insulin-PI3K-mTOR pathway. J Cell Mol Med. 2015;19(6):1174–82.PubMedPubMedCentralCrossRef
11.
go back to reference Tyagi S, Singh N, Virdi JK, Jaggi AS. Diabetes abolish cardioprotective effects of remote ischemic conditioning: evidences and possible mechanisms. J Physiol Biochem. 2019;75(1):19–28.PubMedCrossRef Tyagi S, Singh N, Virdi JK, Jaggi AS. Diabetes abolish cardioprotective effects of remote ischemic conditioning: evidences and possible mechanisms. J Physiol Biochem. 2019;75(1):19–28.PubMedCrossRef
12.
go back to reference Ardehali H, Chen Z, Ko Y, Mejía-Alvarez R, Marbán E. Multiprotein complex containing succinate dehydrogenase confers mitochondrial ATP-sensitive K+ channel activity. Proc Natl Acad Sci USA. 2004;101(32):11880–5.PubMedCrossRefPubMedCentral Ardehali H, Chen Z, Ko Y, Mejía-Alvarez R, Marbán E. Multiprotein complex containing succinate dehydrogenase confers mitochondrial ATP-sensitive K+ channel activity. Proc Natl Acad Sci USA. 2004;101(32):11880–5.PubMedCrossRefPubMedCentral
13.
go back to reference Hamel D, Sanchez M, Duhamel F, et al. G-protein-coupled receptor 91 and succinate are key contributors in neonatal postcerebral hypoxia-ischemia recovery. Arterioscler Thromb Vasc Biol. 2014;34(2):285–93.PubMedCrossRef Hamel D, Sanchez M, Duhamel F, et al. G-protein-coupled receptor 91 and succinate are key contributors in neonatal postcerebral hypoxia-ischemia recovery. Arterioscler Thromb Vasc Biol. 2014;34(2):285–93.PubMedCrossRef
14.
go back to reference Yu L, Liang H, Dong X, et al. Reduced silent information regulator 1 signaling exacerbates myocardial ischemia-reperfusion injury in type 2 diabetic rats and the protective effect of melatonin. J Pineal Res. 2015;59(3):376–90.PubMedCrossRef Yu L, Liang H, Dong X, et al. Reduced silent information regulator 1 signaling exacerbates myocardial ischemia-reperfusion injury in type 2 diabetic rats and the protective effect of melatonin. J Pineal Res. 2015;59(3):376–90.PubMedCrossRef
15.
go back to reference Grimm S. Respiratory chain complex II as general sensor for apoptosis. Biochim Biophys Acta. 2013;1827(5):565–72.PubMedCrossRef Grimm S. Respiratory chain complex II as general sensor for apoptosis. Biochim Biophys Acta. 2013;1827(5):565–72.PubMedCrossRef
16.
go back to reference Chouchani ET, Pell VR, Gaude E, et al. Ischaemic accumulation of succinate controls reperfusion injury through mitochondrial ROS. Nature. 2014;515(7527):431–5.PubMedPubMedCentralCrossRef Chouchani ET, Pell VR, Gaude E, et al. Ischaemic accumulation of succinate controls reperfusion injury through mitochondrial ROS. Nature. 2014;515(7527):431–5.PubMedPubMedCentralCrossRef
17.
go back to reference Martin JL, Ashji SHC, Gruszczyk AV, et al. Succinate accumulation drives ischaemia-reperfusion injury during organ transplantation. Nat Metab. 2019;1:966–74.PubMedPubMedCentralCrossRef Martin JL, Ashji SHC, Gruszczyk AV, et al. Succinate accumulation drives ischaemia-reperfusion injury during organ transplantation. Nat Metab. 2019;1:966–74.PubMedPubMedCentralCrossRef
18.
go back to reference Kohlhauer M, Pell VR, Burger N, et al. Protection against cardiac ischemia-reperfusion injury by hypothermia and by inhibition of succinate accumulation and oxidation is additive. Basic Res Cardiol. 2019;114(3):18.PubMedPubMedCentralCrossRef Kohlhauer M, Pell VR, Burger N, et al. Protection against cardiac ischemia-reperfusion injury by hypothermia and by inhibition of succinate accumulation and oxidation is additive. Basic Res Cardiol. 2019;114(3):18.PubMedPubMedCentralCrossRef
19.
go back to reference Cao S, Liu Y, Wang H, et al. Ischemic postconditioning influences electron transport chain protein turnover in Langendorff-perfused rat hearts. PeerJ. 2016;4:e1706.PubMedPubMedCentralCrossRef Cao S, Liu Y, Wang H, et al. Ischemic postconditioning influences electron transport chain protein turnover in Langendorff-perfused rat hearts. PeerJ. 2016;4:e1706.PubMedPubMedCentralCrossRef
20.
go back to reference Shi Z, Fu F, Yu L, et al. Vasonatrin peptide attenuates myocardial ischemia-reperfusion injury in diabetic rats and underlying mechanisms. Am J Physiol Heart Circ Physiol. 2015;308(4):H281–90.PubMedCrossRef Shi Z, Fu F, Yu L, et al. Vasonatrin peptide attenuates myocardial ischemia-reperfusion injury in diabetic rats and underlying mechanisms. Am J Physiol Heart Circ Physiol. 2015;308(4):H281–90.PubMedCrossRef
22.
go back to reference Charan K, Goyal A, Gupta JK, Yadav HN. Role of atrial natriuretic peptide in ischemic preconditioning-induced cardioprotection in the diabetic rat heart. J Surg Res. 2016;201(2):272–8.PubMedCrossRef Charan K, Goyal A, Gupta JK, Yadav HN. Role of atrial natriuretic peptide in ischemic preconditioning-induced cardioprotection in the diabetic rat heart. J Surg Res. 2016;201(2):272–8.PubMedCrossRef
23.
go back to reference Kloner RA, Schwartz LL. State of the science of cardioprotection: challenges and opportunities–proceedings of the 2010 NHLBI Workshop on cardioprotection. J Cardiovasc Pharmacol Ther. 2011;16(3–4):223–32.PubMedCrossRef Kloner RA, Schwartz LL. State of the science of cardioprotection: challenges and opportunities–proceedings of the 2010 NHLBI Workshop on cardioprotection. J Cardiovasc Pharmacol Ther. 2011;16(3–4):223–32.PubMedCrossRef
24.
go back to reference Murphy E, Steenbergen C. Ion transport and energetics during cell death and protection. Physiology (Bethesda). 2008;23:115–23. Murphy E, Steenbergen C. Ion transport and energetics during cell death and protection. Physiology (Bethesda). 2008;23:115–23.
25.
go back to reference Sanada S, Komuro I, Kitakaze M. Pathophysiology of myocardial reperfusion injury: preconditioning, postconditioning, and translational aspects of protective measures. Am J Physiol Heart Circ Physiol. 2011;301(5):H1723–41.PubMedCrossRef Sanada S, Komuro I, Kitakaze M. Pathophysiology of myocardial reperfusion injury: preconditioning, postconditioning, and translational aspects of protective measures. Am J Physiol Heart Circ Physiol. 2011;301(5):H1723–41.PubMedCrossRef
26.
go back to reference Zhao ZQ, Corvera JS, Halkos ME, et al. Inhibition of myocardial injury by ischemic postconditioning during reperfusion: comparison with ischemic preconditioning. Am J Physiol Heart Circ Physiol. 2003;285(2):H579–88.PubMedCrossRef Zhao ZQ, Corvera JS, Halkos ME, et al. Inhibition of myocardial injury by ischemic postconditioning during reperfusion: comparison with ischemic preconditioning. Am J Physiol Heart Circ Physiol. 2003;285(2):H579–88.PubMedCrossRef
27.
go back to reference Lambert EA, Thomas CJ, Hemmes R, et al. Sympathetic nervous response to ischemia-reperfusion injury in humans is altered with remote ischemic preconditioning. Am J Physiol Heart Circ Physiol. 2016;311(2):H364–70.PubMedCrossRef Lambert EA, Thomas CJ, Hemmes R, et al. Sympathetic nervous response to ischemia-reperfusion injury in humans is altered with remote ischemic preconditioning. Am J Physiol Heart Circ Physiol. 2016;311(2):H364–70.PubMedCrossRef
28.
go back to reference Donato M, Goyeneche MA, Garces M, et al. Myocardial triggers involved in activation of remote ischaemic preconditioning. Exp Physiol. 2016;101(6):708–16.PubMedCrossRef Donato M, Goyeneche MA, Garces M, et al. Myocardial triggers involved in activation of remote ischaemic preconditioning. Exp Physiol. 2016;101(6):708–16.PubMedCrossRef
29.
go back to reference Zhu J, Yao K, Wang Q, et al. Ischemic Postconditioning-regulated miR-499 protects the rat heart against ischemia/reperfusion injury by inhibiting apoptosis through PDCD4. Cell Physiol Biochem. 2016;39(6):2364–80.PubMedCrossRef Zhu J, Yao K, Wang Q, et al. Ischemic Postconditioning-regulated miR-499 protects the rat heart against ischemia/reperfusion injury by inhibiting apoptosis through PDCD4. Cell Physiol Biochem. 2016;39(6):2364–80.PubMedCrossRef
30.
go back to reference Hu J, Gu XY, Meng Y, et al. Effect of dexmedetomidine postconditioning on myocardial ischemia-reperfusion injury and inflammatory response in diabetic rats. Nan Fang Yi Ke Da Xue Xue Bao. 2017;37(11):1506–11.PubMed Hu J, Gu XY, Meng Y, et al. Effect of dexmedetomidine postconditioning on myocardial ischemia-reperfusion injury and inflammatory response in diabetic rats. Nan Fang Yi Ke Da Xue Xue Bao. 2017;37(11):1506–11.PubMed
31.
go back to reference Shen Y, Liu X, Shi J, Wu X. Involvement of Nrf2 in myocardial ischemia and reperfusion injury. Int J Biol Macromol. 2019;125:496–502.PubMedCrossRef Shen Y, Liu X, Shi J, Wu X. Involvement of Nrf2 in myocardial ischemia and reperfusion injury. Int J Biol Macromol. 2019;125:496–502.PubMedCrossRef
32.
go back to reference Xu J, Lin C, Wang T, Zhang P, Liu Z, Lu C. Ergosterol attenuates LPS-induced myocardial injury by modulating oxidative stress and apoptosis in rats. Cell Physiol Biochem. 2018;48(2):583–92.PubMedCrossRef Xu J, Lin C, Wang T, Zhang P, Liu Z, Lu C. Ergosterol attenuates LPS-induced myocardial injury by modulating oxidative stress and apoptosis in rats. Cell Physiol Biochem. 2018;48(2):583–92.PubMedCrossRef
33.
go back to reference Sun F, Huo X, Zhai Y, et al. Crystal structure of mitochondrial respiratory membrane protein complex II. Cell. 2005;121(7):1043–57.PubMedCrossRef Sun F, Huo X, Zhai Y, et al. Crystal structure of mitochondrial respiratory membrane protein complex II. Cell. 2005;121(7):1043–57.PubMedCrossRef
34.
go back to reference Dhingra R, Kirshenbaum LA. Succinate dehydrogenase/complex II activity obligatorily links mitochondrial reserve respiratory capacity to cell survival in cardiac myocytes. Cell Death Dis. 2015;6:e1956.PubMedPubMedCentralCrossRef Dhingra R, Kirshenbaum LA. Succinate dehydrogenase/complex II activity obligatorily links mitochondrial reserve respiratory capacity to cell survival in cardiac myocytes. Cell Death Dis. 2015;6:e1956.PubMedPubMedCentralCrossRef
35.
36.
go back to reference Guo L, Zhou D, Wu D, et al. Short-term remote ischemic conditioning may protect monkeys after ischemic stroke. Ann Clin Transl Neurol. 2019;6(2):310–23.PubMedPubMedCentralCrossRef Guo L, Zhou D, Wu D, et al. Short-term remote ischemic conditioning may protect monkeys after ischemic stroke. Ann Clin Transl Neurol. 2019;6(2):310–23.PubMedPubMedCentralCrossRef
37.
go back to reference Krásnik V, Štefaničková J, Fabková J, Bucková D, Helbich M. [Prevalence of the diabetic retinopathy and genetic factors significance in the development of diabetic retinopathy in patients with diabetes mellitus type I and II in Slovakia (DIARET SK study). Overview of Actual Findings and Design of the Epidemiological DIARET SK Study]. Cesk Slov Oftalmol. 2015. 71(5): 237–42. Krásnik V, Štefaničková J, Fabková J, Bucková D, Helbich M. [Prevalence of the diabetic retinopathy and genetic factors significance in the development of diabetic retinopathy in patients with diabetes mellitus type I and II in Slovakia (DIARET SK study). Overview of Actual Findings and Design of the Epidemiological DIARET SK Study]. Cesk Slov Oftalmol. 2015. 71(5): 237–42.
38.
go back to reference Pælestik KB, Jespersen NR, Jensen RV, Johnsen J, Bøtker HE, Kristiansen SB. Effects of hypoglycemia on myocardial susceptibility to ischemia-reperfusion injury and preconditioning in hearts from rats with and without type 2 diabetes. Cardiovasc Diabetol. 2017;16(1):148.PubMedPubMedCentralCrossRef Pælestik KB, Jespersen NR, Jensen RV, Johnsen J, Bøtker HE, Kristiansen SB. Effects of hypoglycemia on myocardial susceptibility to ischemia-reperfusion injury and preconditioning in hearts from rats with and without type 2 diabetes. Cardiovasc Diabetol. 2017;16(1):148.PubMedPubMedCentralCrossRef
39.
go back to reference Marfella R, D’Amico M, Di FC, et al. Myocardial infarction in diabetic rats: role of hyperglycaemia on infarct size and early expression of hypoxia-inducible factor 1. Diabetologia. 2002;45(8):1172–81.PubMedCrossRef Marfella R, D’Amico M, Di FC, et al. Myocardial infarction in diabetic rats: role of hyperglycaemia on infarct size and early expression of hypoxia-inducible factor 1. Diabetologia. 2002;45(8):1172–81.PubMedCrossRef
40.
go back to reference Kristiansen SB, Pælestik KB, Johnsen J, et al. Impact of hyperglycemia on myocardial ischemia-reperfusion susceptibility and ischemic preconditioning in hearts from rats with type 2 diabetes. Cardiovasc Diabetol. 2019;18(1):66.PubMedPubMedCentralCrossRef Kristiansen SB, Pælestik KB, Johnsen J, et al. Impact of hyperglycemia on myocardial ischemia-reperfusion susceptibility and ischemic preconditioning in hearts from rats with type 2 diabetes. Cardiovasc Diabetol. 2019;18(1):66.PubMedPubMedCentralCrossRef
41.
go back to reference Jensen RV, Zachara NE, Nielsen PH, Kimose HH, Kristiansen SB, Bøtker HE. Impact of O-GlcNAc on cardioprotection by remote ischaemic preconditioning in non-diabetic and diabetic patients. Cardiovasc Res. 2013;97(2):369–78.PubMedCrossRef Jensen RV, Zachara NE, Nielsen PH, Kimose HH, Kristiansen SB, Bøtker HE. Impact of O-GlcNAc on cardioprotection by remote ischaemic preconditioning in non-diabetic and diabetic patients. Cardiovasc Res. 2013;97(2):369–78.PubMedCrossRef
42.
go back to reference Jones SP, Zachara NE, Ngoh GA, et al. Cardioprotection by N-acetylglucosamine linkage to cellular proteins. Circulation. 2008;117(9):1172–82.PubMedCrossRef Jones SP, Zachara NE, Ngoh GA, et al. Cardioprotection by N-acetylglucosamine linkage to cellular proteins. Circulation. 2008;117(9):1172–82.PubMedCrossRef
43.
go back to reference Zhang Y, Zhang L, Gu E, Zhu B, Zhao X, Chen J. Long-term insulin treatment restores cardioprotection induced by sufentanil postconditioning in diabetic rat heart. Exp Biol Med (Maywood). 2016;241(6):650–7.CrossRef Zhang Y, Zhang L, Gu E, Zhu B, Zhao X, Chen J. Long-term insulin treatment restores cardioprotection induced by sufentanil postconditioning in diabetic rat heart. Exp Biol Med (Maywood). 2016;241(6):650–7.CrossRef
44.
go back to reference Xu J, Pan H, Xie X, Zhang J, Wang Y, Yang G. Inhibiting succinate dehydrogenase by dimethyl malonate alleviates brain damage in a rat model of cardiac arrest. Neuroscience. 2018;393:24–32.PubMedCrossRef Xu J, Pan H, Xie X, Zhang J, Wang Y, Yang G. Inhibiting succinate dehydrogenase by dimethyl malonate alleviates brain damage in a rat model of cardiac arrest. Neuroscience. 2018;393:24–32.PubMedCrossRef
45.
go back to reference Jespersen NR, Hjortbak MV, Lassen TR, et al. Cardioprotective effect of succinate dehydrogenase inhibition in rat hearts and human myocardium with and without diabetes mellitus. Sci Rep. 2020;10(1):10344.PubMedPubMedCentralCrossRef Jespersen NR, Hjortbak MV, Lassen TR, et al. Cardioprotective effect of succinate dehydrogenase inhibition in rat hearts and human myocardium with and without diabetes mellitus. Sci Rep. 2020;10(1):10344.PubMedPubMedCentralCrossRef
46.
go back to reference Drzewoski J, Watala C. Is aspirin resistance a real problem in people with type 2 diabetes. Diabetes Care. 2004;27(5):1245–6.PubMedCrossRef Drzewoski J, Watala C. Is aspirin resistance a real problem in people with type 2 diabetes. Diabetes Care. 2004;27(5):1245–6.PubMedCrossRef
47.
go back to reference Nicolucci A, De Berardis G, Sacco M, Tognoni G. AHA/ADA vs ESC/EASD recommendations on aspirin as a primary prevention strategy in people with diabetes: how the same data generate divergent conclusions. Eur Heart J. 2007;28(16):1925–7.PubMedCrossRef Nicolucci A, De Berardis G, Sacco M, Tognoni G. AHA/ADA vs ESC/EASD recommendations on aspirin as a primary prevention strategy in people with diabetes: how the same data generate divergent conclusions. Eur Heart J. 2007;28(16):1925–7.PubMedCrossRef
48.
go back to reference Bouman HJ, Schömig E, van Werkum JW, et al. Paraoxonase-1 is a major determinant of clopidogrel efficacy. Nat Med. 2011;17(1):110–6.PubMedCrossRef Bouman HJ, Schömig E, van Werkum JW, et al. Paraoxonase-1 is a major determinant of clopidogrel efficacy. Nat Med. 2011;17(1):110–6.PubMedCrossRef
49.
go back to reference Sacco RL, Sivenius J, Diener HC. Efficacy of aspirin plus extended-release dipyridamole in preventing recurrent stroke in high-risk populations. Arch Neurol. 2005;62(3):403–8.PubMedCrossRef Sacco RL, Sivenius J, Diener HC. Efficacy of aspirin plus extended-release dipyridamole in preventing recurrent stroke in high-risk populations. Arch Neurol. 2005;62(3):403–8.PubMedCrossRef
50.
go back to reference Yang XM, Liu Y, Cui L, et al. Two classes of anti-platelet drugs reduce anatomical infarct size in monkey hearts. Cardiovasc Drugs Ther. 2013;27(2):109–15.PubMedCrossRef Yang XM, Liu Y, Cui L, et al. Two classes of anti-platelet drugs reduce anatomical infarct size in monkey hearts. Cardiovasc Drugs Ther. 2013;27(2):109–15.PubMedCrossRef
51.
go back to reference Cohen MV, Downey JM. Combined cardioprotectant and antithrombotic actions of platelet P2Y12 receptor antagonists in acute coronary syndrome: just what the doctor ordered. J Cardiovasc Pharmacol Ther. 2014;19(2):179–90.PubMedCrossRef Cohen MV, Downey JM. Combined cardioprotectant and antithrombotic actions of platelet P2Y12 receptor antagonists in acute coronary syndrome: just what the doctor ordered. J Cardiovasc Pharmacol Ther. 2014;19(2):179–90.PubMedCrossRef
52.
go back to reference Cohen MV, Yang XM, White J, Yellon DM, Bell RM, Downey JM. Cangrelor-mediated cardioprotection requires platelets and sphingosine phosphorylation. Cardiovasc Drugs Ther. 2016;30(2):229–32.PubMedCrossRef Cohen MV, Yang XM, White J, Yellon DM, Bell RM, Downey JM. Cangrelor-mediated cardioprotection requires platelets and sphingosine phosphorylation. Cardiovasc Drugs Ther. 2016;30(2):229–32.PubMedCrossRef
53.
go back to reference Tuncay E, Okatan EN, Vassort G, Turan B. ß-blocker timolol prevents arrhythmogenic Ca2+ release and normalizes Ca2+ and Zn2+ dyshomeostasis in hyperglycemic rat heart. PLoS ONE. 2013;8(7):e71014.PubMedPubMedCentralCrossRef Tuncay E, Okatan EN, Vassort G, Turan B. ß-blocker timolol prevents arrhythmogenic Ca2+ release and normalizes Ca2+ and Zn2+ dyshomeostasis in hyperglycemic rat heart. PLoS ONE. 2013;8(7):e71014.PubMedPubMedCentralCrossRef
54.
go back to reference Sun JY, Zhai L, Li QL, et al. Effects of ACE inhibition on endothelial progenitor cell mobilization and prognosis after acute myocardial infarction in type 2 diabetic patients. Clinics (Sao Paulo). 2013;68(5):665–73.CrossRef Sun JY, Zhai L, Li QL, et al. Effects of ACE inhibition on endothelial progenitor cell mobilization and prognosis after acute myocardial infarction in type 2 diabetic patients. Clinics (Sao Paulo). 2013;68(5):665–73.CrossRef
55.
go back to reference Werner N, Priller J, Laufs U, et al. Bone marrow-derived progenitor cells modulate vascular reendothelialization and neointimal formation: effect of 3-hydroxy-3-methylglutaryl coenzyme a reductase inhibition. Arterioscler Thromb Vasc Biol. 2002;22(10):1567–72.PubMedCrossRef Werner N, Priller J, Laufs U, et al. Bone marrow-derived progenitor cells modulate vascular reendothelialization and neointimal formation: effect of 3-hydroxy-3-methylglutaryl coenzyme a reductase inhibition. Arterioscler Thromb Vasc Biol. 2002;22(10):1567–72.PubMedCrossRef
56.
go back to reference Dimmeler S, Aicher A, Vasa M, et al. HMG-CoA reductase inhibitors (statins) increase endothelial progenitor cells via the PI 3-kinase/Akt pathway. J Clin Invest. 2001;108(3):391–7.PubMedPubMedCentralCrossRef Dimmeler S, Aicher A, Vasa M, et al. HMG-CoA reductase inhibitors (statins) increase endothelial progenitor cells via the PI 3-kinase/Akt pathway. J Clin Invest. 2001;108(3):391–7.PubMedPubMedCentralCrossRef
Metadata
Title
The disappearance of IPO in myocardium of diabetes mellitus rats is associated with the increase of succinate dehydrogenase-flavin protein
Authors
Mengyuan Deng
Wei Chen
Haiying Wang
Yan Wang
Wenjing Zhou
Tian Yu
Publication date
01-12-2021
Publisher
BioMed Central
Published in
BMC Cardiovascular Disorders / Issue 1/2021
Electronic ISSN: 1471-2261
DOI
https://doi.org/10.1186/s12872-021-01949-z

Other articles of this Issue 1/2021

BMC Cardiovascular Disorders 1/2021 Go to the issue