polydatin/infarction

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Cardioprotective effect of polydatin on ventricular remodeling after myocardial infarction in coronary artery ligation rats.

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The purpose of this study was to explore the effect of polydatin on ventricular remodeling after myocardial infarction in coronary artery ligation rats and to elucidate the underlying mechanisms. A rat model of ventricular remodeling after myocardial infarction was established by left coronary

Polydatin protects against acute myocardial infarction-induced cardiac damage by activation of Nrf2/HO-1 signaling.

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Polydatin is a traditional Chinese medicine that provides myocardial protection after acute myocardial infarction (AMI). The study aim was to investigate the myocardial protection polydatin in H9c2 myocardial cells cultured in a hypoxic atmosphere and in a rat AMI model induced by ligating the left

Polydatin protects cardiomyocytes against myocardial infarction injury by activating Sirt3.

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Myocardial infarction (MI), which is characterized by chamber dilation and left ventricular (LV) dysfunction, represents a major cause of morbidity and mortality worldwide. Polydatin (PD), a monocrystalline and polyphenolic drug isolated from a traditional Chinese herb (Polygonum cuspidatum),

Polydatin protects H9c2 cells from hypoxia-induced injury via up-regulating long non-coding RNA DGCR5.

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Polydatin (PD), a monocrystalline polyphenolic drug mainly found in the roots of Polygonum cuspidatum, has various pharmacological activities. Long non-coding RNAs (lncRNA) DiGeorge syndrome critical region gene 5 (DGCR5) was found to participate in the suppression of multiple cancers. Here, we

trans-Polydatin protects the mouse heart against ischemia/reperfusion injury via inhibition of the renin-angiotensin system (RAS) and Rho kinase (ROCK) activity.

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BACKGROUND Recent studies highlighted the protective benefits of a Chinese herb extract from polygonum cuspidatum, trans-polydatin, on cardiac disease. We investigated the therapeutic effect of trans-polydatin on myocardial ischemia/reperfusion (IR) injury and the underlying mechanisms related to

Polydatin ameliorates diabetic cardiomyopathy via Sirt3 activation.

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Diabetic cardiomyopathy is identified as cardiac ventricular dysfunction induced by an insulin shortage in diabetic patients. Our previous studies have shown that Polydatin (PD) alleviates cardiac dysfunction after myocardial infarction (MI) injury. Nevertheless, the mechanism by which PD regulates

Cardioprotective effect of polydatin against ischemia/reperfusion injury: roles of protein kinase C and mito K(ATP) activation.

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Polydatin preconditioning (PPC) has been reported to be protective against brain and intestine ischemia/reperfusion injury (I/R injury), but whether polydatin exerts cardioprotective effect against myocardial ischemia/reperfusion and the underlying mechanisms remain unclear. Previous studies have

MALAT1 Up-Regulator Polydatin Protects Brain Microvascular Integrity and Ameliorates Stroke Through C/EBPβ/MALAT1/CREB/PGC-1α/PPARγ Pathway.

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Metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) is a long non-coding RNA contributing to protect the blood-brain barrier (BBB) after stroke. We searched for small molecules that may up-regulate MALAT1 and focused on polydatin (PD), a natural product, as a possible candidate. PD

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

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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

Polydatin post-treatment alleviates myocardial ischaemia/reperfusion injury by promoting autophagic flux.

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Polydatin (PD), a resveratrol (RES) glycoside, has a stronger antioxidative effect than RES. It is known that RES is an autophagic enhancer and exerts a cardioprotective effect against ischaemia/reperfusion (I/R) injury. However, the effect of PD post-treatment on myocardial I/R injury remains

Protective effect of polydatin against ischemia/reperfusion injury in rat heart.

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The aim of the present study was to investigate the protective effect of polydatin against myocardial ischemia/reperfusion injury in rats and the underlying mechanism. In anesthetized rats, ischemia and reperfusion arrhythmia produced by ligating and loosing the coronary artery was recorded and

Involvement of cell adhesion molecules in polydatin protection of brain tissues from ischemia-reperfusion injury.

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Previous studies have demonstrated that polydatin, a crystal component extracted from the root stem of the perennial herbage Polygonum Cuspidatum Sieb.et Zucc, exerts a neuroprotective effect on cerebral injury induced by ischemia/reperfusion. To investigate the possible mechanism of this action, we

Effect of polydatin on expression of p53 and Notch1 in brain tissue of ischemic cerebrovascular disease.

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Secondary injury of brain tissue following cerebral infarction exhibits a complicated pathogenesis that is attributed to the induction of apoptosis and inflammatory response. The present study aimed to investigate the polydatin neuroprotective effects and their mode of action in cerebral ischemic

Polydatin modulates inflammation by decreasing NF-κB activation and oxidative stress by increasing Gli1, Ptch1, SOD1 expression and ameliorates blood-brain barrier permeability for its neuroprotective effect in pMCAO rat brain.

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Inflammation and oxidative stress play an important role in cerebral ischemic pathogenesis. Polydatin has been proved to elicit numerous biological effects through its anti-inflammatory and anti-oxidant properties. However, little is known regard to the mechanism of polydatin's neuroprotection in

Neuroprotective effects of polydatin against mitochondrial-dependent apoptosis in the rat cerebral cortex following ischemia/reperfusion injury.

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The neuroprotective effect of polydatin (PD) against hemorrhagic shock-induced mitochondrial injury has been described previously, and mitochondrial dysfunction and apoptosis were reportedly involved in ischemic stroke. In the present study the neuroprotective effect of PD in preventing apoptosis

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