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      Hawthorn Leaf Flavonoids Protect against Diabetes-Induced Cardiomyopathy in Rats via PKC- α Signaling Pathway

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          Abstract

          Objectives

          DCM has become one of the main reasons of death in diabetic patients. In this study, we aimed to explore the hawthorn leaf flavonoids (HLF) protective effect against diabetes-induced cardiac injury and the underlying mechanisms in experimental rats.

          Methods

          Experimental diabetic model was induced by intraperitoneal injection of streptozotocin (STZ, 40 mg/kg) in rats after feeding with high-fat diet for 8 weeks. The diabetic rats received a 16-week treatment of different doses of HLF (50, 100, and 200). The morphological changes of myocardial cells were observed by light microscope; the concentration of antioxidant indicator and TNF- α and the expression of PKC- α mRNA, PKC- α, and NF- κB proteins were assessed as well.

          Results

          STZ-induced diabetes mellitus prompted blood glucose, cardiac injury, oxidative stress, and inflammation, accompanied with suppressed body weight. On the contrary, HLF administration improved body weight and blood glucose and attenuated myocardial structural abnormalities in diabetic rats. In addition, HLF decreased MDA level and enhanced SOD activities, inhibited TNF- α expression, and downregulated PKC- α mRNA, PKC- α, and NF- κB which were induced by diabetes.

          Conclusions

          HLF has a protective effect against diabetic cardiomyopathy in rats. The mechanism may be involved in reducing oxidative stress and inflammation via inactivation of the PKC- α signaling pathway.

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          Most cited references 31

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          Diabetic cardiomyopathy: mechanisms and new treatment strategies targeting antioxidant signaling pathways.

          Cardiovascular disease is the primary cause of morbidity and mortality among the diabetic population. Both experimental and clinical evidence suggest that diabetic subjects are predisposed to a distinct cardiomyopathy, independent of concomitant macro- and microvascular disorders. 'Diabetic cardiomyopathy' is characterized by early impairments in diastolic function, accompanied by the development of cardiomyocyte hypertrophy, myocardial fibrosis and cardiomyocyte apoptosis. The pathophysiology underlying diabetes-induced cardiac damage is complex and multifactorial, with elevated oxidative stress as a key contributor. We now review the current evidence of molecular disturbances present in the diabetic heart, and their role in the development of diabetes-induced impairments in myocardial function and structure. Our focus incorporates both the contribution of increased reactive oxygen species production and reduced antioxidant defenses to diabetic cardiomyopathy, together with modulation of protein signaling pathways and the emerging role of protein O-GlcNAcylation and miRNA dysregulation in the progression of diabetic heart disease. Lastly, we discuss both conventional and novel therapeutic approaches for the treatment of left ventricular dysfunction in diabetic patients, from inhibition of the renin-angiotensin-aldosterone-system, through recent evidence favoring supplementation of endogenous antioxidants for the treatment of diabetic cardiomyopathy. Novel therapeutic strategies, such as gene therapy targeting the phosphoinositide 3-kinase PI3K(p110α) signaling pathway, and miRNA dysregulation, are also reviewed. Targeting redox stress and protective protein signaling pathways may represent a future strategy for combating the ever-increasing incidence of heart failure in the diabetic population. Copyright © 2014 Elsevier Inc. All rights reserved.
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            Diabetic cardiomyopathy: insights into pathogenesis, diagnostic challenges, and therapeutic options.

            Diabetic cardiomyopathy is the presence of myocardial dysfunction in the absence of coronary artery disease and hypertension. Hyperglycemia seems to be central to the pathogenesis of diabetic cardiomyopathy and to trigger a series of maladaptive stimuli that result in myocardial fibrosis and collagen deposition. These processes are thought to be responsible for altered myocardial relaxation characteristics and manifest as diastolic dysfunction on imaging. Sophisticated imaging technologies also have permitted the detection of subtle systolic dysfunction in the diabetic myocardium. In the early stages, these changes appear reversible with tight metabolic control, but as the pathologic processes become organized, the changes are irreversible and contribute to an excess risk of heart failure among diabetic patients independently of common comorbidities, such as coronary artery disease and hypertension. Therapeutic agents specifically targeting processes that lead to these pathophysiologic changes are in the early stages of development. Although glycemic control and early administration of neurohormonal antagonists remain the cornerstones of therapeutic approaches, newer treatment targets are currently being explored.
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              The metabolic syndrome: inflammation, diabetes mellitus, and cardiovascular disease.

              There is accumulating evidence that inflammation is an important risk factor in cardiovascular disease (CVD). Elevated levels of the inflammatory marker high-sensitivity C-reactive protein (hs-CRP) are associated with increased risk for CVD and diabetes mellitus. Adding hs-CRP to the definition of the metabolic syndrome has been shown to improve the prediction of CVD. Elevated hs-CRP levels may also be predictive of development of the metabolic syndrome. Current definitions of the metabolic syndrome differ, and cardiovascular risk appears to differ according to which component risk factors are present. Further studies are required to identify a widely accepted criterion for the syndrome that will optimally predict the risk of diabetes and CVD. It is possible that such a definition will include a measure of inflammation.
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                Author and article information

                Contributors
                Journal
                Evid Based Complement Alternat Med
                Evid Based Complement Alternat Med
                ECAM
                Evidence-based Complementary and Alternative Medicine : eCAM
                Hindawi
                1741-427X
                1741-4288
                2017
                4 October 2017
                : 2017
                Affiliations
                Department of Pharmacology, School of Pharmacy, Hubei University of Science and Technology, Xianning 437100, China
                Author notes

                Academic Editor: I-Min Liu

                Article
                10.1155/2017/2071952
                5646339
                Copyright © 2017 Qing Min et al.

                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.

                Funding
                Funded by: Hubei Provincial Health Department
                Award ID: 2012Z-B02
                Funded by: Hubei University of Science and Technology
                Award ID: ZX1017
                Categories
                Research Article

                Complementary & Alternative medicine

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