2,3,5,4′-Tetrahydroxystilbene-2-O-β-D-glucoside protects murine hearts against ischemia/reperfusion injury by activating Notch1/Hes1 signaling and attenuating endoplasmic reticulum stress

Zhang, Meng; Yu, Liming; Zhao, Hang; Zhou, Xiuping; Yang, Qian; Fan, ST; Li, Yan; Zhai, Mengen; Li, Bu-ying; Zhang, Bin; Jin, Zhenxiao; Duan, Weixun; Wang, Siwang

doi:10.1038/aps.2016.144

Cited by 21 publications

(17 citation statements)

References 62 publications

(53 reference statements)

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“…After the induction of diabetes, 210 SD rats were randomly assigned to the following groups: the sham group, which received the same operation except that the suture around the left anterior descending coronary artery was left untied; the MI/R + V group, which was orally treated with vehicle (distilled water, 0.5 mL/d) for 3 consecutive days and once again right before the MI/R operation; the MI/R + PD group, which was orally treated with polydatin (PD, Aladdin Chemicals, Shanghai, China; 20 mg/kg/d) for 3 consecutive days and once again right before the MI/R operation; the MI/R + PD + DAPT group, which was treated with polydatin (as above) and DAPT (Santa Cruz, CA, USA; 50 mg/kg, intraperitoneally, 20 min before the beginning of myocardial reperfusion); the MI/R + PD + LY group, which was treated with polydatin (as above) and LY294002 (LY, Santa Cruz, CA, USA; 30 mg/kg, intraperitoneally, 20 min before the beginning of myocardial reperfusion); the sham + DAPT group, which received sham operation and DAPT injection (as above); and the sham + LY group, which received sham operation and LY injection (as above). The dosages of polydatin and exogenous inhibitors were chosen based on previous publications [ 11 , 12 , 18 , 19 , 23 , 24 ]. MI/R surgery was carried out as described previously [ 23 ].…”

Section: Methodsmentioning

confidence: 99%

Polydatin Protects Diabetic Heart against Ischemia‐Reperfusion Injury via Notch1/Hes1‐Mediated Activation of Pten/Akt Signaling

Dong

et al. 2018

Oxidative Medicine and Cellular Longevity

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Diabetes exacerbates oxidative/nitrative stress during myocardial ischemia-reperfusion (MI/R) injury. Recent studies highlighted the cardioprotective actions of polydatin. However, its effect on diabetic MI/R injury and the underlying mechanisms remain unknown. This work was undertaken to evaluate the effect of polydatin on diabetic MI/R injury with a focus on Notch1/Hes1 signaling and myocardial oxidative/nitrative stress. Streptozotocin- (STZ-) induced diabetic rats were administered with polydatin (20 mg/kg/d) in the absence or presence of DAPT (a γ-secretase inhibitor) or LY294002 (a PI3K/Akt inhibitor) and then subjected to MI/R injury. Polydatin administration preserved cardiac function and reduced myocardial infarct size. Moreover, polydatin ameliorated myocardial oxidative/nitrative stress damage as evidenced by decreased myocardial superoxide generation, malondialdehyde, gp91phox expression, iNOS expression, NO metabolite level, and nitrotyrosine content and increased eNOS phosphorylation. However, these effects were blocked by DAPT administration. DAPT also inhibited the stimulatory effect of polydatin on the Notch1/Hes1-Pten/Akt signaling pathway in a diabetic myocardium. Additionally, LY294002 not only abolished polydatin's antiapoptotic effect but also reversed its inhibitory effect on myocardial oxidative/nitrative stress. Polydatin effectively reduced MI/R injury and improved left ventricular functional recovery under diabetic condition by ameliorating oxidative/nitrative stress damage. Importantly, Notch1/Hes1-mediated activation of Pten/Akt signaling played a crucial role in this process.

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Section: Methodsmentioning

confidence: 99%

Polydatin Protects Diabetic Heart against Ischemia‐Reperfusion Injury via Notch1/Hes1‐Mediated Activation of Pten/Akt Signaling

Dong

et al. 2018

Oxidative Medicine and Cellular Longevity

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“…Cell viability was measured as previously described [ 60 ]. The cells were initially seeded in 96-well culture plates (1 × 10 4 per well).…”

Section: Methodsmentioning

confidence: 99%

Diallyl trisulfide exerts cardioprotection against myocardial ischemia-reperfusion injury in diabetic state, role of AMPK-mediated AKT/GSK-3β/HIF-1α activation

Dong

et al. 2017

Oncotarget

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Diallyl trisulfide (DATS), the major active ingredient in garlic, has been reported to confer cardioprotective effects. However, its effect on myocardial ischemia-reperfusion (MI/R) injury in diabetic state and the underlying mechanism are still unknown. We hypothesize that DATS reduces MI/R injury in diabetic state via AMPK-mediated AKT/GSK-3β/HIF-1α activation. Streptozotocin-induced diabetic rats received MI/R surgery with or without DATS (20mg/kg) treatment in the presence or absence of Compound C (Com.C, an AMPK inhibitor, 0.25mg/kg) or LY294002 (a PI3K inhibitor, 5mg/kg). We found that DATS significantly improved heart function and reduced myocardial apoptosis. Additionally, in cultured H9c2 cells, DATS (10μM) also attenuated simulated ischemia-reperfusion injury. We found that AMPK and AKT/GSK-3β/HIF-1α signaling were down-regulated under diabetic condition, while DATS markedly increased the phosphorylation of AMPK, ACC, AKT and GSK-3β as well as HIF-1α expression in MI/R-injured myocardium. However, these protective actions were all blunted by Com.C administration. Additionally, LY294002 abolished the stimulatory effect of DATS on AKT/GSK-3β/HIF-1α signaling without affecting AMPK signaling. While 2-methoxyestradiol (a HIF-1α inhibitor) reduced HIF-1α expression without affecting AKT/GSK-3β signaling. Taken together, these data showed that DATS protected against MI/R injury in diabetic state by attenuating cellular apoptosis via AMPK-mediated AKT/GSK-3β/HIF-1α signaling. Its cardioprotective effect deserves further study.

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“…Resveratrol can attenuate neointimal VSMC hyperplasia in rats, following balloon injury, through a mechanism that involves inhibition of the Notch signaling [303]. Activation of Notch signaling reduces myocardial ischemia reperfusion injury (MI/RI), by activating key components of survival pathways, namely, PI3K-Akt, NOS, and mitochondrial K + -ATP (mitoKATP) channels [231]; BBR, polydatin, and 2,3,5,4′-tetrahydroxystilbene-2-O-β-D-glucoside upregulate Notch-1/HES1 signaling attenuating myocardial apoptosis both in cultured cardiomyocytes and in rats subjected to MI/RI [304][305][306].…”

Section: Nutraceuticals Acting Through the Notch Pathwaymentioning

confidence: 99%

The Use of Nutraceuticals to Counteract Atherosclerosis: The Role of the Notch Pathway

Aquila

Marracino

Martino

et al. 2019

Oxidative Medicine and Cellular Longevity

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Despite the currently available pharmacotherapies, today, thirty percent of worldwide deaths are due to cardiovascular diseases (CVDs), whose primary cause is atherosclerosis, an inflammatory disorder characterized by the buildup of lipid deposits on the inside of arteries. Multiple cellular signaling pathways have been shown to be involved in the processes underlying atherosclerosis, and evidence has been accumulating for the crucial role of Notch receptors in regulating the functions of the diverse cell types involved in atherosclerosis onset and progression. Several classes of nutraceuticals have potential benefits for the prevention and treatment of atherosclerosis and CVDs, some of which could in part be due to their ability to modulate the Notch pathway. In this review, we summarize the current state of knowledge on the role of Notch in vascular health and its modulation by nutraceuticals for the prevention of atherosclerosis and/or treatment of related CVDs.

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2,3,5,4′-Tetrahydroxystilbene-2-O-β-D-glucoside protects murine hearts against ischemia/reperfusion injury by activating Notch1/Hes1 signaling and attenuating endoplasmic reticulum stress

Cited by 21 publications

References 62 publications

Polydatin Protects Diabetic Heart against Ischemia‐Reperfusion Injury via Notch1/Hes1‐Mediated Activation of Pten/Akt Signaling

Polydatin Protects Diabetic Heart against Ischemia‐Reperfusion Injury via Notch1/Hes1‐Mediated Activation of Pten/Akt Signaling

Diallyl trisulfide exerts cardioprotection against myocardial ischemia-reperfusion injury in diabetic state, role of AMPK-mediated AKT/GSK-3β/HIF-1α activation

The Use of Nutraceuticals to Counteract Atherosclerosis: The Role of the Notch Pathway

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