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      Effects of Dexmedetomidine Postconditioning on Myocardial Ischemia/Reperfusion Injury in Diabetic Rats: Role of the PI3K/Akt-Dependent Signaling Pathway

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          Abstract

          Objective

          The present study was designed to determine whether dexmedetomidine (DEX) exerts cardioprotection against myocardial I/R injury in diabetic hearts and the mechanisms involved.

          Methods

          A total of 30 diabetic rats induced by high-glucose-fat diet and streptozotocin (STZ) were randomly assigned to five groups: diabetic sham-operated group (DM-S), diabetic I/R group (DM-I/R), diabetic DEX group (DM-D), diabetic DEX + Wort group (DM-DW), and diabetic Wort group (DM-W). Another 12 age-matched male normal SD rats were randomly divided into two groups: sham-operated group (S) and I/R group (I/R). All rats were subjected to 30 min myocardial ischemia followed by 120 min reperfusion except sham groups. Plasmas were collected to measure the malondialdehyde (MDA), creatine kinase isoenzymes (CK-MB), and lactate dehydrogenase (LDH) levels and superoxide dismutase (SOD) activity at the end of reperfusion. Pathologic changes in myocardial tissues were observed by H-E staining. The total and phosphorylated form of Akt and GSK-3 β protein expressions were measured by western blot. The ratio of Bcl-2/Bax at mRNA level was detected by reverse transcription-polymerase chain reaction (RT-PCR).

          Results

          DEX significantly reduced plasma CK-MB, MDA concentration, and LDH level and increased SOD activity caused by I/R. The phosphorylation of Akt and GSK-3 β was increased, Bcl-2 mRNA and the Bcl-2/Bax ratio was increased, and Bax mRNA was decreased in the DEX group as compared to the I/R group, while posttreatment with Wort attenuated the effects induced by DEX.

          Conclusion

          The results of this study suggest that DEX postconditioning may increase the phosphorylation of GSK-3 β by activating the PI3K/Akt signaling pathway and may inhibit apoptosis and oxidative stress of the myocardium, thus exerting protective effects in diabetic rat hearts suffering from I/R injury.

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          Most cited references36

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          Impact of Diabetes on Cardiovascular Disease: An Update

          Alessandra Saldanha de Mattos Matheus, Lucianne Tannus, Roberta Arnoldi Cobas … (2013)
          Cardiovascular diseases are the most prevalent cause of morbidity and mortality among patients with type 1 or type 2 diabetes. The proposed mechanisms that can link accelerated atherosclerosis and increased cardiovascular risk in this population are poorly understood. It has been suggested that an association between hyperglycemia and intracellular metabolic changes can result in oxidative stress, low-grade inflammation, and endothelial dysfunction. Recently, epigenetic factors by different types of reactions are known to be responsible for the interaction between genes and environment and for this reason can also account for the association between diabetes and cardiovascular disease. The impact of clinical factors that may coexist with diabetes such as obesity, dyslipidemia, and hypertension are also discussed. Furthermore, evidence that justify screening for subclinical atherosclerosis in asymptomatic patients is controversial and is also matter of this review. The purpose of this paper is to describe the association between poor glycemic control, oxidative stress, markers of insulin resistance, and of low-grade inflammation that have been suggested as putative factors linking diabetes and cardiovascular disease.
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            The role of oxidative stress in the pathogenesis of type 2 diabetes mellitus micro- and macrovascular complications: avenues for a mechanistic-based therapeutic approach.

            Giovanna Muscogiuri, Alberto Davalli, Paolo Fanti … (2011)
            A growing body of evidence suggests that oxidative stress plays a key role in the pathogenesis of micro- and macrovascular diabetic complications. The increased oxidative stress in subjects with type 2 diabetes is a consequence of several abnormalities, including hyperglycemia, insulin resistance, hyperinsulinemia, and dyslipidemia, each of which contributes to mitochondrial superoxide overproduction in endothelial cells of large and small vessels as well as the myocardium. The unifying pathophysiological mechanism that underlies diabetic complications could be explained by increased production of reactive oxygen species (ROS) via: (1) the polyol pathway flux, (2) increased formation of advanced glycation end products (AGEs), (3) increased expression of the receptor for AGEs, (4) activation of protein kinase C isoforms, and (5) overactivity of the hexosamine pathway. Furthermore, the effects of oxidative stress in individuals with type 2 diabetes are compounded by the inactivation of two critical anti-atherosclerotic enzymes: endothelial nitric oxide synthase and prostacyclin synthase. Of interest, the results of clinical trials in patients with type 2 diabetes in whom intensive management of all the components of the metabolic syndrome (hyperglycemia, hypercholesterolemia, and essential hypertension) was attempted (with agents that exert a beneficial effect on serum glucose, serum lipid concentrations, and blood pressure, respectively) showed a decrease in adverse cardiovascular end points. The purpose of this review is (1) to examine the mechanisms that link oxidative stress to micro- and macrovascular complications in subjects with type 2 diabetes and (2) to consider the therapeutic opportunities that are presented by currently used therapeutic agents which possess antioxidant properties as well as new potential antioxidant substances.
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              Oxidative stress and myocardial injury in the diabetic heart.

              David Ansley, Baohua Wang (2012)
              Reactive oxygen or nitrogen species play an integral role in both myocardial injury and repair. This dichotomy is differentiated at the level of species type, amount and duration of free radical generated. Homeostatic mechanisms designed to prevent free radical generation in the first instance, scavenge, or enzymatically convert them to less toxic forms and water, playing crucial roles in the maintenance of cellular structure and function. The outcome between functional recovery and dysfunction is dependent upon the inherent ability of these homeostatic antioxidant defences to withstand acute free radical generation, in the order of seconds to minutes. Alternatively, pre-existent antioxidant capacity (from intracellular and extracellular sources) may regulate the degree of free radical generation. This converts reactive oxygen and nitrogen species to the role of second messenger involved in cell signalling. The adaptive capacity of the cell is altered by the balance between death or survival signal converging at the level of the mitochondria, with distinct pathophysiological consequences that extends the period of injury from hours to days and weeks. Hyperglycaemia, hyperlipidaemia and insulin resistance enhance oxidative stress in the diabetic myocardium that cannot adapt to ischaemia-reperfusion. Altered glucose flux, mitochondrial derangements and nitric oxide synthase uncoupling in the presence of decreased antioxidant defence and impaired prosurvival cell signalling may render the diabetic myocardium more vulnerable to injury, remodelling and heart failure. Copyright © 2012 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd.
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                Author and article information

                Contributors
                Qin Gao:
                ORCID: http://orcid.org/0000-0002-7599-4295
                Zhenghong Li:
                ORCID: http://orcid.org/0000-0003-0905-7743
                Journal
                Journal ID (nlm-ta): J Diabetes Res
                Journal ID (iso-abbrev): J Diabetes Res
                Journal ID (publisher-id): JDR
                Title: Journal of Diabetes Research
                Publisher: Hindawi
                ISSN (Print): 2314-6745
                ISSN (Electronic): 2314-6753
                Publication date Collection: 2018
                Publication date (Electronic): 8 October 2018
                Volume: 2018
                Electronic Location Identifier: 3071959
                Affiliations
                1Department of Anesthesiology, The First Affiliated Hospital of Bengbu Medical College, Bengbu, Anhui 233004, China
                2Department of Physiology, Bengbu Medical College, Bengbu, Anhui 233030, China
                Author notes

                Academic Editor: Larissa Pernomian

                Author information
                http://orcid.org/0000-0002-7599-4295
                http://orcid.org/0000-0003-0905-7743
                Article
                DOI: 10.1155/2018/3071959
                PMC ID: 6196799
                SO-VID: 0cc62989-4f17-449b-ab20-fcbbd93b7ddc
                Copyright © Copyright © 2018 Xiangyang Cheng et al.
                License:

                This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                Date received : 12 May 2018
                Date accepted : 17 July 2018
                Funding
                Funded by: Bengbu Medical College
                Award ID: Byycx1625
                Award ID: BYKF1786
                Funded by: Anhui Provincial Education Department Project
                Award ID: KJ2018A0212
                Funded by: Natural Science Foundation of Anhui Province
                Award ID: 1508085MH170
                Award ID: 1508085MH169
                Funded by: National Natural Science Foundation of China
                Award ID: 81770297
                Categories
                Subject: Research Article

                Data availability:

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