Myricetin Possesses Potential Protective Effects on Diabetic Cardiomyopathy through Inhibiting IκBα/NFκB and Enhancing Nrf2/HO‐1

Liao, Hai‐Han; Zhu, Jinxiu; Hong, Feng; Ni, Jian; Zhang, Nan; Chen, Si; Liu, Huang-Jun; Zheng, Yang; Deng, Wei; Tang, Qi‐Zhu

doi:10.1155/2017/8370593

Cited by 70 publications

(60 citation statements)

References 31 publications

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“…Our present study indicated that myricetin diminished HG‐induced caspase‐3 activation in HUVECs. Our results were supported by the study of Liao et al [2017] indicating that myricetin decreased the expression of caspase‐3 and protected cardiomyocytes from oxidative damage and apoptosis caused by streptozotocin . In one study, it has been shown that myricetin inhibited activation of caspase‐3 and prevented glutamate‐induced neuronal cell death …”

Section: Discussionsupporting

confidence: 88%

Myricetin ameliorates high glucose‐induced endothelial dysfunction in human umbilical vein endothelial cells

Aminzadeh

Bashiri

2019

Cell Biochemistry & Function

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Endothelial dysfunction is recognized as the initial detectable stage of cardiovascular disease, a serious complication of diabetes. In this study, we evaluated effects of myricetin on high glucose (HG)-elicited oxidative damage in human umbilical vein endothelial cells (HUVECs). The cells were pre-incubated with myricetin and then treated with HG to induce apoptosis. The effect of myricetin on viability was investigated by MTT assay. The levels of lipid peroxidation (LPO) were determined by thiobarbituric acid (TBA) method. The protein expression of Bax, Bcl-2 and caspase-3 was measured by western blot analysis. Moreover, the effect of myricetin on total antioxidant capacity (TAC) and total thiol molecules was also determined.Our results showed that myricetin was able to markedly restore the viability of endothelial cells under oxidative stress. Myricetin reduced HG-caused increase in LPO levels. Also, TAC and total thiol molecules were notably elevated by myricetin.Incubation with myricetin decreased the protein expression levels of Bax, whereas it increased the expression levels of the Bcl-2, compared with HG treatment alone.Furthermore, myricetin significantly decreased cleaved caspase-3 protein expression. It is concluded that myricetin may protect HUVECs from oxidative stress induced by HG via increasing cell TAC and reducing Bax/Bcl-2 protein ratio, and caspase-3 expression.

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Section: Discussionsupporting

confidence: 88%

Myricetin ameliorates high glucose‐induced endothelial dysfunction in human umbilical vein endothelial cells

Aminzadeh

Bashiri

2019

Cell Biochemistry & Function

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“…As inflammation was involved in the development of DCM ( Liao et al, 2017 ; Wang et al, 2018 ), we evaluated the expression of tumor necrosis factor (TNF-α) using IHC staining ( Figure 5A ). The protein levels of TNF-α in the diabetic hearts was increased compared with the NDM group, whereas it was ameliorated in the DM+PKK group.…”

Section: Resultsmentioning

confidence: 99%

Exogenous Pancreatic Kallikrein Improves Diabetic Cardiomyopathy in Streptozotocin-Induced Diabetes

Yang

Wang

et al. 2018

Front. Pharmacol.

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Aims: To evaluate the protective effects of exogenous pancreatic kallikrein (PKK) treatment on diabetic cardiomyopathy (DCM) and explore the underlying mechanisms.Methods and Results: Streptozotocin (STZ)-induced diabetic rats, a type 1 diabetic model, were treated with either PKK or saline for 12 weeks. Non-diabetic rats were used as controls. PKK administration attenuated the mitochondria swelling, Z line misalignments, myofibrosis and interstitial collagen accumulation in diabetic myocardial tissue. The oxidative stress imbalance including increased nitrotyrosine, decreased anti-oxidative components such as nuclear receptor nuclear factor like 2 (Nrf2), glutathione peroxidase 1(GPx-1), catalase (CAT) and superoxide dismutase (SOD), were recovered in the heart of PKK-treated diabetic rats. In diabetic rats, protein expression of TGF-β1 and accumulation of collagen I in the heart tissues was decreased after PKK administration. Markers for inflammation were decreased in diabetic rats by PKK treatment. Compared to diabetic rats, PKK reversed the degradation of IκB-α, an inhibitive element of heterotrimer nuclear factor kappa B (NF-κB). The endothelial nitric oxide synthase (eNOS) protein and myocardial nitrate/nitrite were impaired in the heart of diabetic rats, which, however, were restored after PKK treatment. The sarcoplasmic reticulum Ca2+-ATPase 2 (SERCA2) and phospholamban (PLN) were mishandled in diabetic rats, while were rectified in PKK-treated diabetic rats. The plasma NT-proBNP level was increased in diabetic rats while was reduced with PKK treatment.Conclusion: PKK protects against DCM via reducing fibrosis, inflammation, and oxidative stress, promoting nitric oxide production, as well as restoring the function of the calcium channel.

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“…Myricetin also exhibited diabetic nephrotoxic activity in rats and improved carbohydrate metabolism, which subsequently enhanced glucose utilization and renal function in STZ-Cd-induced DN rats (Kandasamy and Ashokkumar, 2014). Liao HH demonstrated that myricetin attenuated DCM-associated cardiac injury in mice treated with STZ and that myricetin exerts potential protective effects on diabetic cardiomyopathy by inhibiting IκBα/NFκB and enhancing Nrf2/HO-1 in neonatal rat cardiomyocytes (Liao et al, 2017).…”

Section: Myricetin and Dihydromyricetinmentioning

confidence: 98%

Antidiabetic Potential of Flavonoids from Traditional Chinese Medicine: A Review

Bai

et al. 2019

Am. J. Chin. Med.

162

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Diabetes mellitus (DM) is a group of metabolic disorders in which high blood sugar levels occur over a prolonged period. Approximately 4% of the global population is affected by DM. Western medical treatment methods for diabetes including injection or oral hypoglycemic drugs have some toxic or side effects, economic pressures, and so on. Many researchers turn to discover new drugs from natural products or Traditional Chinese Medicine (TCM). Flavonoids are widely distributed in plants, and many studies have shown that flavonoids possess antidiabetic properties, exhibiting not only well-recognized antidiabetic and hypoglycemic activities but also activity in the treatment of diabetic complications. In this review, we systematically summarized anti-diabetic flavonoid compounds based on structure classification by examining the PubMed, Springer Link, Web of Science, and CNKI databases. There are 13 flavonoid compounds listed which have been studied extensively and have antidiabetic features respectively. Apigenin, baicalein, and catechin mainly reduces blood glucose via anti-oxidation; hesperidin is good for diabetic neuropathy; glycyrrhiza flavonoids have a significant effect on gestational DM; quercetin takes advantage of crossing the blood–brain barrier and improving renal function. Some compounds have protective and preventive effects on diabetic complications, such as kaempferol and puerarin which are beneficial to cardiomyopathy; myricetin has therapeutic potential in the treatment of DN; dihydromyricetin might improve CI. It is a pity or might be a pointcut that most studies remain in the animal experimental stage, and further investigation should be carried out.

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Myricetin Possesses Potential Protective Effects on Diabetic Cardiomyopathy through Inhibiting IκBα/NFκB and Enhancing Nrf2/HO‐1

Cited by 70 publications

References 31 publications

Myricetin ameliorates high glucose‐induced endothelial dysfunction in human umbilical vein endothelial cells

Myricetin ameliorates high glucose‐induced endothelial dysfunction in human umbilical vein endothelial cells

Exogenous Pancreatic Kallikrein Improves Diabetic Cardiomyopathy in Streptozotocin-Induced Diabetes

Antidiabetic Potential of Flavonoids from Traditional Chinese Medicine: A Review

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