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adenosine 5 monophosphate/инфаркт
Линкът е запазен в клипборда
Страница 1 от 16 резултата
Effect of Yiqihuoxue prescription on myocardial energy metabolism after myocardial infarction via cross talk of liver kinase B1-dependent Notch1 and adenosine 5'-monophosphate-activated protein kinase.
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Stomatin-like protein-2 relieve myocardial ischemia/reperfusion injury by adenosine 5'-monophosphate-activated protein kinase signal pathway.
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Previous studies have shown that stomatin-like protein-2 (SLP-2) could regulate mitochondrial biogenesis and function. The study was designed to explore the contribution of SLP-2 to the myocardial ischemia and reperfusion (I/R) injury. Anesthetized rats were treated with SLP-2 and subjected to
When hypothermia meets hypotension and hyperglycemia: the diverse effects of adenosine 5'-monophosphate on cerebral ischemia in rats.
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Mild hypothermia renders potent neuroprotection against acute brain injury. Recent reports show that adenosine 5'-monophosphate (AMP) plays a role in thermoregulation and induces hypothermia in mice. Therefore, this study sought to determine whether AMP induces hypothermia in rats and to study its
MicroRNA-338-5p alleviates cerebral ischemia/reperfusion injury by targeting connective tissue growth factor through the adenosine 5'-monophosphate-activated protein kinase/mammalian target of rapamycin signaling pathway.
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Cerebral ischemia/reperfusion (CIR) injury could lead to the function of brain cell disorder and cerebral infarction. MicroRNAs (miRNAs) have been reported to participate in the progression and protection of CIR injury. Thus, our study aimed to investigate the functional effects of microRNA-338-5p
Cannabinoid receptor 2 deletion deteriorates myocardial infarction through the down-regulation of AMPK-mTOR-p70S6K signaling-mediated autophagy.
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Cannabinoid receptor 2 (CB2R) has been reported to play an important role in the regulation of pathogenesis and progression of myocardial infarction (MI). Here we tried to investigate its potential mechanisms. The ratio of infarct size in heart issue was detected by TTC staining, and cardiac
Preconditioning induces sustained neuroprotection by downregulation of adenosine 5'-monophosphate-activated protein kinase.
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Ischemic preconditioning (IPC) induces endogenous neuroprotection from a subsequent ischemic injury. IPC involves downregulation of metabolic pathways. As adenosine 5'-monophosphate-activated protein kinase (AMPK) is a critical sensor of energy balance and plays a major role in cellular metabolism,
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
Pretreatment of rats with increased bioavailable berberine attenuates cerebral ischemia-reperfusion injury via down regulation of adenosine-5'monophosphate kinase activity.
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Berberine (BBR) exhibits multiple beneficial biological effects. However, poor bioavailability of BBR has limited its clinical application. We previously demonstrated that solid dispersion of BBR with sodium caprate (HGSD) remarkably improves its bioavailability. We examined whether this increased
Diosmetin alleviates hypoxia‑induced myocardial apoptosis by inducing autophagy through AMPK activation
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Diosmetin has shown great potential in the control of several diseases. The aim of the present study was to evaluate the role of diosmetin as a candidate agent for the treatment of myocardial infarction which was mainly caused by hypoxia. The model of hypoxia‑injured myocardial cells was established
Dexmedetomidine protects mice against myocardium ischaemic/reperfusion injury by activating an AMPK/PI3K/Akt/eNOS pathway.
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Acute myocardial ischaemia/reperfusion (MIR) injury leads to severe arrhythmias and has a high rate of lethality. In the present study, we aim to determine the effect of dexmedetomidine (Dex) on heart injury parameters following MIR surgery. We examined the effects of Dex on heart function
Metformin attenuated endotoxin-induced acute myocarditis via activating AMPK.
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Metformin is a widely used anti-diabetic drug and increasing evidence suggests that metformin have profound cardioprotective effects under both diabetic and non-diabetic situations. The protective benefits of metformin have been proved in diabetic patients with cardiovascular complications and in
Dexmedetomidine Exerted Anti-arrhythmic Effects in Rat With Ischemic Cardiomyopathy via Upregulation of Connexin 43 and Reduction of Fibrosis and Inflammation.
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Mesenchymal stem cells attenuate blood-brain barrier leakage after cerebral ischemia in mice.
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BACKGROUND
Ischemic stroke induced matrixmetallo-proteinase-9 (MMP-9) upregulation, which increased blood-brain barrier permeability. Studies demonstrated that mesenchymal stem cell therapy protected blood-brain barrier disruption from several cerebrovascular diseases. However, the underlying
Effects of metformin in experimental stroke.
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OBJECTIVE
Adenosine 5'-monophosphate-activated protein kinase (AMPK) is an important sensor of energy balance. Stroke-induced AMPK activation is deleterious because both pharmacological inhibition and genetic deletion of AMPK are neuroprotective. Metformin is a known AMPK activator but reduces
Exosomes from mesenchymal stem cells overexpressing MIF enhance myocardial repair.
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Accumulating evidence has shown that mesenchymal stem cell (MSC)-derived exosomes (exo) mediate cardiac repair following myocardial infarction (MI). Macrophage migration inhibitory factor (MIF), a proinflammatory cytokine, plays a critical role in regulating cell homeostasis. This study aimed to
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