Methanolic seed extract of Vitis vinifera ameliorates oxidative stress, inflammation and ATPase dysfunction in infarcted and non-infarcted heart of streptozotocin–nicotinamide induced male diabetic rats

Giribabu, Nelli; Roslan, Josef; Rekha, S.; Salleh, Naguib

doi:10.1016/j.ijcard.2016.07.250

Cited by 25 publications

(13 citation statements)

References 41 publications

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“…Diabetes activates the NF-kB signaling, which regulates the expression of several genes involved in the inflammatory response and cellular stress including iNOS 53 , 54 . Levels of inflammation in heart of diabetic rats were high as evidenced from the elevated levels of NF-κβ and iNOS 55 , 56 . NF-κB is activated by hyperglycemia or free radical linking oxidative damage and inflammation where increased expression of iNOS catalyzed the production of large amount of NO 9 .…”

Section: Discussionmentioning

confidence: 99%

“…Diabetes-induced heart damage, apoptosis and fibrosis are the most prominent feature in diabetic animals 55 , 56 , 62 , 63 . In this study, histopathological changes indicating of tissue injury were noted in diabetic rat heart including degeneration, inflammation, positive expression of caspase-3, induced level of cardiac pro-apoptotic markers (cleaved caspase-3 and Bax) and the inhibition of anti-apoptotic marker (Bcl-2) in the heart of diabetic rats.…”

Section: Discussionmentioning

confidence: 99%

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Mechanistic insights into the augmented effect of bone marrow mesenchymal stem cells and thiazolidinediones in streptozotocin-nicotinamide induced diabetic rats

Hamza

Fikry

Abdallah

et al. 2018

Sci Rep

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This study was designed to assess whether the protective effects of bone marrow-derived mesenchymal stem cells (MSCs) against diabetes could be enhanced by pioglitazone (PIO), a PPARγ agonist. Combined MSCs and PIO treatments markedly improved fasting blood glucose, body weight, lipid profile levels, insulin level, insulin resistance, β cell function. Those protective effects also attenuated both pancreatic lesions and fibrosis in diabetic rats and decreased the depletion of pancreatic mediators of glycemic and lipid metabolism including peroxisome proliferator-activated receptor alpha (PPARα), PGC-1α, GLP-1 and IRS-2. Cardiac biogenesis of diabetic groups was also improved with MSCs and/or PIO treatments as reflected by the enhanced up-regulation of the expressions of cardiac IRS1, Glucose transporter 4, PGC-1, PPARα and CPT-1 genes and the down-regulated expression of lipogenic gene SREBP. The combination of MSCs and PIO also potentiated the decrease of abnormal myocardial pathological lesions in diabetic rats. Similarly, the inhibitory effects of MSCs on diabetic cardiac fibrosis and on the up regulations of TGF-β, collagen I and III gene expressions were partial but additive when combined with PIO. Therefore, combined therapy with PIO and BMCs transplantation could further potentiate the protective benefit of MSCs against diabetes and cardiac damage compared to MSCs monotherapy.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Mechanistic insights into the augmented effect of bone marrow mesenchymal stem cells and thiazolidinediones in streptozotocin-nicotinamide induced diabetic rats

Hamza

Fikry

Abdallah

et al. 2018

Sci Rep

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“…STZ induced a significant increase in plasma troponin I and CK-MB, while TQ counteracted the oxidative injuries in cardiac muscles due to STZ. Giribabu et al [ 27 ] stated that STZ-nicotinamide-induced cardiac injuries were accompanied by significant increases in troponin I and CK-MB in diabetic rats. On the contrary, TQ ameliorated the cardiac injuries that occurred in diabetic rats through hindering inflammatory progression and enhancing antioxidant status [ 28 ].…”

Section: Discussionmentioning

confidence: 99%

Thymoquinone Attenuates Cardiomyopathy in Streptozotocin‐Treated Diabetic Rats

Atta

El‐Far

Farrag

et al. 2018

Oxidative Medicine and Cellular Longevity

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Diabetic cardiomyopathy is a diabetic complication due to oxidative stress injuries. This study examined the protecting influence of thymoquinone (TQ) on diabetes-caused cardiac complications. The intracellular means by which TQ works against diabetes-caused cardiac myopathy in rats is not completely understood. In this study, Wistar male rats (n = 60) were assigned into four groups: control, diabetic (diabetes induced by IP infusion of streptozotocin, 65 mg/kg), diabetic + TQ (diabetic rats given TQ (50 mg/kg) administered once per day by stomach gavage), and TQ (50 mg/kg) for 12 weeks. TQ supplementation appreciably recovered the cardiac parameters alongside significant declines in plasma nitric oxide concentrations and total superoxide dismutase (T.SOD) activities. Importantly, TQ downgraded expression of cardiac-inducible nitric oxide synthase in addition to significantly upregulating vascular endothelial growth factor and erythropoietin genes and nuclear factor-erythroid-2-related factor 2 (Nrf2) protein. TQ normalized plasma triacylglycerol and low-density lipoprotein-cholesterol and significantly improved the high-density lipoprotein-cholesterol levels. Additionally, TQ administration improved the antioxidant ability of cardiac tissue via significantly increased cardiac T.SOD and decreased cardiac malondialdehyde levels. Oral supplementation with TQ prevented diabetic-induced cardiomyopathy via its inhibitory effect on the E-selectin level, C-reactive protein, and interleukin-6. The TQ protecting effect on the heart tissue was shown by normalization of the plasma cardiac markers troponin I and creatine kinase. This experiment shows the aptitude of TQ to protect cardiac muscles against diabetic oxidative stress, mainly through upregulation of Nrf2, which defeated oxidative damage by improvement of the antioxidant power of cardiac muscle that consequently protected the cardiac muscles and alleviated the inflammatory process.

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“…Myocardial infarction (MI) was induced in 18 male diabetic rats by injecting isoproterenol (ISO) subcutaneously at a dose of 85 mg/kg on Days 41 and 42 (Giribabu, Roslan, Rekha, & Salleh, 2016;Khalil et al, 2015).…”

Section: Induction Of Myocardial Infarctionmentioning

confidence: 99%

The protective effect of kaempferol on heart via the regulation of Nrf2, NF‐κβ, and PI3K/Akt/GSK‐3β signaling pathways in isoproterenol‐induced heart failure in diabetic rats

Zhang

Guo

Wang

et al. 2019

Drug Development Research

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This study was designed to delineate the effect of kaempferol (KF) on heart failure (HF) in diabetic rats. Streptozotocin‐induced male diabetic rats received KF orally at 10 and 20 mg/kg for 42 consecutive days. In last 2 days of the experimental period, isoproterenol was subcutaneously injected at 85 mg/kg to induce HF. The hearts were processed for hemodynamic, biochemical, molecular, and histological investigations. Systolic blood pressure, diastolic blood pressure, and mean arterial blood pressure were elevated in KF‐treated HF‐induced diabetic rats. Moreover, KF treatment resulted in decreased fasting blood glucose and glycosylated hemoglobin levels with increased serum insulin levels. Besides, serum cardiac injury markers like troponin‐I, creatine kinase‐muscle/brain, lactate dehydrogenase, and brain natriuretic peptide levels were significantly reduced in KF treatment. KF treatment has shown decrease in cardiac heme oxygenase‐1, nuclear factor erythroid 2–related factor 2 (Nrf‐2), and γ‐glutamylcysteine synthetase with increased Keap1 mRNA levels. The cardioprotection of KF was improved by inhibition of apoptosis via blocking phosphorylation of Akt/glycogen synthase kinase (GSK)‐3β and p38 mitogen‐activated protein‐kinase/extracellular signal‐regulated kinases signaling pathways in HF‐induced diabetic rats. Moreover, reduced cardiac apoptosis in KF treatment was confirmed by decreased terminal deoxynucleotidyl transferase dUTP nick‐end labeling (TUNEL) positive cells, histopathological changes in HF‐induced diabetic rats. Therefore, the cardioprotective effect of KF is attributed to the regulation of Nrf2, nuclear factor kappa‐light‐chain‐enhancer of activated B cells, and Akt/GSK‐3β signaling pathways in HF‐induced diabetic rats.

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Methanolic seed extract of Vitis vinifera ameliorates oxidative stress, inflammation and ATPase dysfunction in infarcted and non-infarcted heart of streptozotocin–nicotinamide induced male diabetic rats

Cited by 25 publications

References 41 publications

Mechanistic insights into the augmented effect of bone marrow mesenchymal stem cells and thiazolidinediones in streptozotocin-nicotinamide induced diabetic rats

Mechanistic insights into the augmented effect of bone marrow mesenchymal stem cells and thiazolidinediones in streptozotocin-nicotinamide induced diabetic rats

Thymoquinone Attenuates Cardiomyopathy in Streptozotocin‐Treated Diabetic Rats

The protective effect of kaempferol on heart via the regulation of Nrf2, NF‐κβ, and PI3K/Akt/GSK‐3β signaling pathways in isoproterenol‐induced heart failure in diabetic rats

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