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berberine/инфаркт

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Myocardial Salvaging Effects of Berberine in Experimental Diabetes Co-Existing with Myocardial Infarction.

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BACKGROUND Berberine, an isoquinoline alkaloid isolated from the Berberis aristata, has been shown to display a wide array of pharmacological activities (hypoglycaemic and hypolipidemic). OBJECTIVE The present study was designed to investigate whether these pharmacological properties translate into

[Protective effects of berberine on spontaneous ventricular fibrillation in dogs after myocardial infarction].

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The effects of berberine (Ber 5 mg/kg iv) on ventricular tachyarrhythmias and electrophysiologic consequences in both normal and ischemic myocardium were studied in the open-chest dogs subjected to programmed electrical stimulation (PES) and intimal surface anodal direct current stimulation of the

Berberine elicits anti-arrhythmic effects via IK1/Kir2.1 in the rat type 2 diabetic myocardial infarction model.

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The purpose of this study was to explore the anti-arrhythmic mechanisms of berberine in diabetic rats with myocardial infarction. Sixty rats were divided into four groups: (1) normal control; (2) myocardial infarction group (MI); (3) Type 2 diabetes with myocardial infarction group (T2DM+MI); and

Liposome encapsulated berberine treatment attenuates cardiac dysfunction after myocardial infarction.

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Inflammation is a known mediator of adverse ventricular remodeling after myocardial infarction (MI) that may lead to reduction of ejection fraction and subsequent heart failure. Berberine is a isoquinoline quarternary alkaloid from plants that has been associated with anti-inflammatory,

Berberine attenuates adverse left ventricular remodeling and cardiac dysfunction after acute myocardial infarction in rats: role of autophagy.

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The present study aimed to test the hypothesis that berberine, a plant-derived anti-oxidant, attenuates adverse left ventricular remodelling and improves cardiac function in a rat model of myocardial infarction (MI). Furthermore, the potential mechanisms that mediated the cardioprotective actions of

Berberine inhibits cardiac remodeling of heart failure after myocardial infarction by reducing myocardial cell apoptosis in rats.

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The effects of berberine on cardiac function of heart failure after myocardial infarction and its possible mechanism were investigated. The anterior descending branches of 50 female Wistar rats were ligatured to establish the model of heart failure after myocardial infarction. At 4 weeks after

Neuroprotective effects of berberine on stroke models in vitro and in vivo.

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Berberine is an alkaloid derived from herb medicine Coptidis Rhizom. Although there are increasing evidences that berberine exhibits neuroprotective effects against ischemic brain damage, little is known about the mechanism. In this study, we investigated the effect of berberine on ischemic injury

[Collagen protein expressions in ischemic myocardium of rats with acute myocardial infarction and effects of qi-tonifying, yin-tonifying and blood-activating herbs and detoxifying and blood-activating herbs].

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OBJECTIVE To investigate collagen protein expressions in ischemic myocardium of rats with acute myocardial infarction (AMI) and the effects of qi-tonifying, yin-tonifying and blood-activating herbs and detoxifying and blood-activating herbs. METHODS AMI model of Wistar rat was established by

Berberine ameliorates neonatal necrotizing enterocolitis by activating the phosphoinositide 3-kinase/protein kinase B signaling pathway.

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Neonatal necrotizing enterocolitis (NEC) is a severe acquired disease that predominantly affects the small intestine of neonates. NEC is caused by a combination of metabolic products, dysfunctions of the blood vessels, mucus and other unknown factors. Berberine may induce beneficial effects on
Objective: It has been shown that angiogenesis is a desirable treatment for patients with ischemic heart disease. We set out to investigate the impact of high-intensity interval training (HIIT) and berberine supplementation on the gene

Berberine attenuates ischemia-reperfusion injury via regulation of adenosine-5'-monophosphate kinase activity in both non-ischemic and ischemic areas of the rat heart.

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BACKGROUND Berberine exhibits numerous pharmacological effects, but the mechanism for its protective effects against ischemia-reperfusion cardiac injury is unknown. METHODS Male Wistar rats were treated with berberine (100 mg/Kg/day, ig) for 14 days and controls treated with water. Hearts were

CPU86017, a berberine derivative, attenuates cardiac failure through normalizing calcium leakage and downregulated phospholamban and exerting antioxidant activity.

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OBJECTIVE To investigate whether CPU86017, a berberine derivative, attenuates heart failure by blocking calcium influx and exerting its antioxidant activity. METHODS Myocardial infarction was induced in male Sprague-Dawley rats for 17 d followed by isoproterenol (ISO) (5 mg/kg, sc) treatment for 5 d
Berberine (BBR) has a variety of pharmacological activities and is widely used in Asian countries. However, the clinical application of BBR still lacks scientific basis, what protective mechanism of BBR against myocardial ischemia-reperfusion injury (MIRI). In vitro experiments, BBR

Pretreatment with a combination of ligustrazine and berberine improves cardiac function in rats with coronary microembolization.

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OBJECTIVE We have shown that a combination of ligustrazine and berberine produces more effective inhibition on platelet activation and inflammatory reactions in rat acute myocardial infarction compared with either agent alone. In this study we evaluated the beneficial effects of a combination of

Neuroprotection of early and short-time applying berberine in the acute phase of cerebral ischemia: up-regulated pAkt, pGSK and pCREB, down-regulated NF-κB expression, ameliorated BBB permeability.

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BACKGROUND Berberine (BBR) has gained attention for its vast beneficial biological effects through immunomodulation, anti-inflammatory and anti-apoptosis properties. Inflammatory and apoptosis damage play an important role in cerebral ischemic pathogenesis and may represent a target for treatment.
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