Abstract Aims Cardiac hypertrophy is characterized by a shift in metabolic substrate utilization, but the molecular events underlying remodelling remain poorly understood. We explored and mitochondrial dysfunction cardiac investigated cardioprotective effects of choline. Methods results The experiments were conducted using model ventricular partially banding abdominal aorta Sprague Dawley rats. Cardiomyocyte size fibrosis significantly increased hypertrophic hearts. In vitro cardiomyocyte...

Background: Acetylcholine (ACh), a neurotransmitter of vagal nerve, offers tolerance to ischemia/reperfusion injury. Given the regulation autophagy in cardioprotection, this study was examine role ACh-elicited protection against hypoxia/reoxygenation (HR) Methods: H9c2 cells were subjected HR Autophagy determined by transmission electron microscopy, MDC staining and western blot. MTT kit, LDH CK release, ATP content TUNEL assay used evaluate cardiomyocytes Atg7 AMPK knockdown performed with...

Mitochondrial biogenesis disorders appear to play an essential role in cardiac dysfunction. Acetylcholine as a potential pharmacologic agent exerts cardioprotective effects. However, its direct action on mitochondria acute damage due ischemia/reperfusion remains unclear. The present study determined the involvement of mitochondrial and function cardiopotection acetylcholine H9c2 cells subjected hypoxia/reoxygenation (H/R). Our findings demonstrated that treatment beginning reoxygenation...

Abstract Mitochondrial dynamics—fission and fusion—are associated with ischaemic heart disease ( IHD ). This study explored the protective effect of vagal nerve stimulation VNS ) against isoproterenol ISO )‐induced myocardial ischaemia in a rat model tested whether plays role preventing disorders mitochondrial dynamics function. Isoproterenol not only caused cardiac injury but also increased expression fission proteins [dynamin‐related peptide1 (Drp1) protein1 (Fis‐1)) decreased fusion...

Aerobic interval training (AIT) can favorably affect cardiovascular diseases. However, the effects of AIT on post-myocardial infarction (MI)—associated mitochondrial dysfunctions remain unclear. In this study, we investigated protective myocardial mitochondria in post-MI rats by focusing dynamics (fusion and fission). Mitochondrial respiratory functions (as measured control ratio (RCR) ADP to oxygen consumption (P/O)); complex activities; dynamic proteins (mitofusin (mfn) 1/2, type 1 optic...

Background: Excessive activation of matrix metalloproteinase 9 (MMP-9) has been found in several inflammatory diseases. Previous studies have shown that acetylcholine (ACh) reduced the levels pro-inflammatory cytokines and decreased tissue damage. Therefore, this study was designed to explore potential effects mechanisms ACh on MMP-9 production cell migration response lipopolysaccharide (LPS) stimulation RAW264.7 cells. Methods: expression activity were induced by LPS cells, examined...

Background: The anti-infammatory and cardioprotective effect of acetylcholine (ACh) has been reported; nevertheless, whether how ACh exhibits an antioxidant property against ischemia/reperfusion (I/R)-induced oxidative stress remains obscure. Methods: In the present study, H9c2 rat cardiomyocytes were exposed to hypoxia/reoxygenation (H/R) mimic I/R injury. We estimated intracellular different sources reactive oxygen species (ROS) by measuring mitochondrial ROS (mtROS), DNA (mtDNA) copy...

Background/Aims: Acetylcholine (ACh) is known to modulate the cardiac redox environment and thereby suppress reactive oxygen species (ROS) generation during oxidative stress. However, there little information about its regulation on ROS clearance. Here we investigate beneficial effects of ACh superoxide dismutase (SOD) as key ROS-detoxifying enzyme system in cultured rat cardiomyoblasts. Methods: H9c2 cells were subjected hypoxia/reoxygenation (H/R) mimic Western blot was used detect...

Phenotypic switching of vascular smooth muscle cells (VSMCs) plays a critical role in atherosclerosis, restenosis, and hypertension. Choline exerts cardioprotective effects; however, little is known about its effects on VSMC phenotypic remodeling. Here, we investigated whether choline modulates changes explored the underlying mechanisms. Approach Results: In cultured VSMCs, promoted Nrf2 (nuclear factor erythroid 2-related 2) nuclear translocation, inducing expression HO-1 (heme oxygenase-1)...

Reactive oxygen species (ROS) production is an important mechanism in myocardial ischemia and nicotinamide adenine dinucleotide phosphate (NADPH) oxidase one of major sources ROS the heart. Previous studies showed that vagus nerve stimulation (VNS) beneficial treating ischemic heart diseases. However, effect VNS on remains elusive. In this study, we investigated role onischemia-induced production. Our results demonstrated alleviated injury, attenuated cardiac dysfunction, reserved...

We explored the role of endoplasmic reticulum (ER)-mitochondria Ca(2+) cross talk involving voltage-dependent anion channel-1 (VDAC1)/glucose-regulated protein 75/inositol 1,4,5-trisphosphate receptor 1 complex and mitofusin 2 in endothelial cells during hypoxia/reoxygenation (H/R), investigated protective effects acetylcholine.Acetylcholine treatment reoxygenation prevented intracellular mitochondrial increases alleviated ER depletion H/R human umbilical vein cells. Consequently,...

To investigate the differentiation of human umbilical cord blood (HUCB)-derived mesenchymal stem cells (MSCs) into hepatocytes by induction fibroblast growth factor-4 (FGF-4) and hepatocyte factor (HGF), to find a new source cell types for therapies hepatic diseases.MSCs were isolated combining gradient density centrifugation with plastic adherence. When HUCB-derived MSCs reached 70% confluence, they cultured in Iscove modified Dulbecco medium (IMDM) supplemented 10 mL/L FBS, 20 ng/mL HGF...

Myocardial infarction (MI) has been shown to induce endothelial dysfunction in peripheral resistance arteries and thus increase resistance. This study was designed investigate the underlying mechanisms of post-MI-related dysfunctional dilatation and, furthermore, examine whether exercise may restore arteries. Adult male Sprague-Dawley rats were divided into three groups: sham-operated, MI, MI + exercise. Ultrastructure relaxation function mesenteric arteries, as well phosphatidylinositol-3...

Summary Aerobic interval training ( AIT ) exerts beneficial effects on cardiovascular disease. However, its cardioprotective mechanisms are not fully understood. The aim of the present study was to evaluate ‐mediated anti‐oxidation by focusing anti‐oxidase and mitochondrial biogenesis in rats after myocardial infarction MI ). Sprague–Dawley were divided into three groups: (i) a sham‐operated control CON ); (ii) an group; (iii) + group. Myocardial microstructure function, markers oxidative...

Abstract Autonomic dysfunction and abnormal immunity lead to systemic inflammatory responses, which result in cardiovascular damage hypertension. The aim of this report was investigate the effects choline on Eight-week-old male spontaneously hypertensive rats (SHRs) Wistar-Kyoto were intraperitoneally injected with or vehicle (8 mg/kg/day). After 8 weeks, restored cardiac function SHRs, as evidenced by decreased heart rate, systolic blood pressure, left ventricle ±dp/dt max increased...

Acetylcholine (ACh) protected against cardiac injury via promoting autophagy and mitochondrial biogenesis, however, the involvement of mitophagy in ACh-elicited cardioprotection remains unknown. In present study, H9c2 cardiomyocytes were subjected to hypoxia/reoxygenation (H/R) ACh treatment during reoxygenation. Mitophagy markers PTEN-induced kinase 1 (PINK1) Parkin translocation examined using western blot confocal fluorescence microscopy. Mitochondrial membrane potential reactive oxygen...

Abstract Cardiac remodeling is characterized by overactivity of the renin–angiotensin system (RAS) and withdrawal vagal activity. We hypothesized that improving activity could attenuate cardiac fibrosis induced angiotensin II (Ang II) in vivo vitro . Rats were subjected to abdominal aorta constriction (AAC) with or without pyridostigmine (PYR) (31 mg/kg/d). After 8 weeks, PYR significantly decreased Ang level, AT1 protein expression collagen deposition tissue improved heart rate variability,...

Nasopharyngeal carcinoma (NPC) is one of the most common malignant tumors in Southern China, especially Guangdong area. To demonstrate a comprehensive profile loss heterozygosity (LOH) NPC, we applied large panel 382 microsatellite polymorphism markers covering all 22 autosomes 98 cases sporadic primary NPC. Of 335 informative markers, 83 loci showed high level LOH (presence equal to or more than 30% cases) and frequent were clustered chromosome 1p36 1p34, 3p14-p21, 3p24-p26, 3q25-q26 3q27,...

1. Acute myocardial infarction (AMI) often activates the sympathetic system and inhibits vagal system. Long-term nerve stimulation (VNS) exerts several beneficial effects on ischaemic heart, including an anti-inflammatory effect. The aim of present study was to investigate whether short-term VNS during AMI could inhibit tumour necrosis factor (TNF)-α expression effect TNF receptor (TNFR), key components in inflammatory responses AMI, a rodent model. 2. Adult male Sprague-Dawley rats were...

Recent findings have reported that up-regulation of tumor necrosis factor-alpha (TNF-α) induced by myocardial hypoxia aggravates cardiomyocyte injury. Acetylcholine (ACh), the principle vagal neurotransmitter, protects cardiomyocytes against inhibiting apoptosis. However, it is still unclear whether ACh regulates TNF-α production in after hypoxia. The concentration extracellular was increased a time-dependent manner during Furthermore, treatment also inhibited hypoxia-induced mRNA and...

Previous findings have shown that acetylcholine (ACh) decreased hypoxia-induced tumor necrosis factor alpha (TNF α) production, thus protected against cardiomyocyte injury. However, whether and how ACh affects TNF α-induced endoplasmic reticulum (ER) stress cell apoptosis remain poorly defined. This study was aimed at determining the effect of in H9c2 cells after α stimulation. Presence ER verified using protein markers glucose regulatory 78 (GRP78) C/EBP homologous (CHOP). Cell by caspase-3...