Qige Huxin Formula Attenuates Isoprenaline-Induced Cardiac Fibrosis in Mice via Modulating Gut Microbiota and Protecting Intestinal Integrity. The composition and metabolic activities of gut microbiota are strongly interconnected with cardiac fibrosis (CF) and heart failure (HF). Qige Huxin formula (QHF), a traditional Chinese medicine (TCM) formulation originating from a classical Fangji Huangqi decoction, has been widely used to clinically treat HF for decades. However, it is still unclear whether QHF alleviates CF by modulating gut microbiota and intestinal integrity. This study aimed to investigate the cardioprotective effects of QHF in isoprenaline-induced CF through modulating gut microbiota and intestinal integrity. Fifty mice were randomly divided into five groups after one week
Dissection of mechanisms of Chinese medicinal formula Si-Miao-Yong-an decoction protects against cardiac hypertrophy and fibrosis in isoprenaline-induced heart failure. Si-Miao-Yong-An decoction (SMYAD) is a traditional Chinese herbal formulation. SMYAD first appeared in the Eastern Han Dynasty according to the "Shen Yi Mi Zhuan". Then the formula was recorded in the "Yan Fang Xin Bian" edited by medical scientist Bao Xiangao in the Qing Dynasty. This well-known prescription has been traditionally used for gangrene and vascular vasculitis. It is mainly used for cardiovascular and endocrine diseases in current clinical applications and research. In this study, the potential mechanisms of SMYAD against cardiac fibrosis and hypertrophy in the β-adrenoceptor agonist isoprenaline induced heart
Protective role of berberine in isoprenaline-induced cardiac fibrosis in rats. Cardiac fibrosis is a crucial aspect of cardiac remodeling that can severely affect cardiac function. Cardiac fibroblasts surely influence this process. Besides, macrophage plays an essential role in cardiac remodeling after heart injury. However, whether macrophage influence fibroblasts remain a question worth exploring. This study aimed to define the role of berberine (BBR) on isoprenaline (ISO)-induced cardiac fibrosis in an in vivo rat model and try to figure out the mechanism in vitro study. The Sprague-Dawley rats were divided into five groups: control group, ISO-treated group, and ISO + BBR (10 mg/kg/d, 30 mg/kg/d, and 60 mg/kg/d orally)-pretreatment groups. Fibrosis was induced by ISO administration (5
Wogonin Attenuates Isoprenaline-Induced Myocardial Hypertrophy in Mice by Suppressing the PI3K/Akt Pathway Many studies have focused on identifying therapeutic targets of myocardial hypertrophy for the treatment of correlative cardiac events. Wogonin is a natural flavonoid compound that displays a potent anti-hypertrophic effect. Knowledge of its pharmacological mechanisms might reveal an effective way to search for therapeutic targets. Myocardial hypertrophy was replicated by the subcutaneous implantation of an isoprenaline mini-pump in mice or isoprenaline treatment of H9C2 cells. Pathologic changes in cardiac structure were assessed by echocardiographic and histological examinations. The signaling transduction in hypertrophy-promoting pathways and the genes involved were detected
Protective effect of scutellarin on myocardial infarction induced by isoprenaline in rats Scutellarin () is the main effective constituent of which has anti-oxidant, anti-apoptotic, anti-inflammatory and other therapeutic properties. The purpose of this study was to investigate the protective effect of on myocardial infarction (MI) induced by isoprenaline (ISO). The rats were subcutaneously
Pharmacological identification of β-adrenoceptor subtypes mediating isoprenaline-induced relaxation of guinea pig colonic longitudinal smooth muscle Object We aimed to identify the β-adrenoceptor (β-AR) subtypes involved in isoprenaline-induced relaxation of guinea pig colonic longitudinal smooth muscle using pharmacological and biochemical approaches. Methods Longitudinal smooth muscle was prepared from the male guinea pig ascending colon and contracted with histamine prior to comparing the relaxant responses to three catecholamines (isoprenaline, adrenaline, and noradrenaline). The inhibitory effects of subtype-selective β-AR antagonists on isoprenaline-induced relaxation were then investigated. Results The relaxant potencies of the catecholamines were ranked as: isoprenaline
Effects of pretreatment with cardiostimulants and beta-blockers on isoprenaline-induced takotsubo-like cardiac dysfunction in rats. Takotsubo syndrome (TS) is an acute cardiac syndrome characterized by regional myocardial akinesia that is not caused by coronary artery occlusion. Exogenous as well as endogenous excess catecholamines can induce TS. The aim of this study was to explore the effects of pharmacological cardio-simulative and cardio-depressing drugs on the development of isoprenaline-induced takotsubo-like cardiac dysfunction, a rat model of TS. We randomized 295 rats into twelve groups. The animals were randomized to pre-treatment with either a low or high dose of metoprolol, propranolol, ICI 118551 (beta-receptor antagonists), milrinone (phosphodiesterase inhibitor), levosimendan or saline
Isoprenaline/β2-AR activates Plexin-A1/VEGFR2 signals via VEGF secretion in gastric cancer cells to promote tumor angiogenesis. The role of stress signals in regulating gastric cancer initiation and progression is not quite clear. It is known that stress signals modulate multiple processes such as immune function, cell migration and angiogenesis. However, few studies have investigated the mechanisms of how stress signals contribute to gastric cancer angiogenesis. Here, we used β2-adrenergic receptor (β2-AR) agonist isoprenaline to imitate a stress signal and demonstrated the molecular mechanism underlying stress's influence on tumor angiogenesis. We found that isoprenaline stimulated vascular endothelial growth factor (VEGF) secretion in gastric cancer cells and plexin-A1 expression
Sugemule-3 Protects against Isoprenaline-induced Cardiotoxicity In vitro Sugemule-3 (SD) is a traditional Chinese medicine with protective effect of myocardium. However, the underlying mechanisms of the effect had not been elucidated. In the present study, the serum of SD was prepared. A model of β-adrenergic agonist isoprenaline (ISO)-induced H9c2 cardiomyocytes injury was established
Coenzyme Q10 prevents oxidative stress and fibrosis in isoprenaline induced cardiac remodeling in aged rats The objective of the present study aimed to investigate the effect of CoQ10 treatment on isoprenaline (ISO)-induced cardiac remodeling in rats. Rats were divided into three groups namely Control group, ISO treated group and CoQ10 + ISO treated group, each consisting of 6 rats. The cardiac
Epinephrine Versus Isoprenaline During Out-of-Hospital Cardiac Arrest With Asystole Background: During out-of-hospital cardiac arrest (OHCA), the patient presents with either a shockable or a non-shockable rhythm. Early cardiopulmonary resuscitation (CPR) and defibrillation of the shockable rhythm may increase chance of survival to more than 50%, however, if untreated, the heart rhythm will deteriorate to a non-shockable rhythm with dismal survival outcomes of 1-5%. Isoprenaline is a pro-arrhythmic drug used to treat bradycardia, and has a structural resemblance to epinephrine, which is the drug of choice during cardiac arrest with non-shockable rhythms. Aims: To evaluate whether intravebous (IV) administration of isoprenaline increases the chance of return of spontaneous circulation (ROSC
Isoprenaline versus nitroglycerine in head-up tilt test HUTT test is used in evaluation of syncope. Isoprenaline and isosorbide dinitrate are used to increase the sensitivity of the test. These drugs act by different mechanisms. We aimed to compare the results of isoprenaline with isosorbide dinitrate. We studied 198 subjects referred for HUTT to our institute; those above the age of 35 years were not included in our study, because isoprenaline was not used commonly above this age; thus, only 90 subjects were analyzed. We found that isosorbide dinitrate resulted in more HUTT-positive results than isoprenaline by absolute risk difference of 26%; relative risk for positive isoprenaline was 60%, confidence interval 0.38-0.93, and P value of 0.03. There was no difference in frequency of types
Spirolactone provides protection from renal fibrosis by inhibiting the endothelial–mesenchymal transition in isoprenaline-induced heart failure in rats Fibrosis results in excessive accumulation of extracellular matrix proteins, collagen component alteration, and abnormalities in structure and is partly derived from a process called the endothelial-mesenchymal transition involving transforming growth factor β (TGF-β). We investigated whether spironolactone, an aldosterone receptor blocker, attenuated isoprenaline (Iso)-induced heart failure in rats and also studied the mechanism for the same. Sprague-Dawley rats were subcutaneously injected with Iso to induce heart failure, which promoted renal fibrosis; rats with spironolactone treatment were given a gavage of spironolactone (30 or 60 mg/kg
Evaluation of cardioprotective effect of aqueous extract of Allium cepa Linn. bulb on isoprenaline-induced myocardial injury in Wistar albino rats To investigate the cardioprotective potential of the aqueous extract of Linn. bulb in isoprenaline-induced myocardial injury in Wistar albino rats. total phenolic, total flavonoid content and 2, 2'-diphenyl-1-picrylhydrazyl hydrate radical scavenging activity was measured. Isoprenaline-induced myocardial injury model was used to evaluate effect of aqueous extract of in Wistar albino rats. Seventy two rats were randomly divided in 6 groups. Rats were treated with 400 mg/kg and 800 mg/kg doses for 30 days and myocardial injury was produced by subcutaneous injection of isoprenaline (ISO) 85 mg/kg on day 28 and 29. Carvedilol 1 mg/kg for 30
MicroRNA-210 Plays a Critical Role in the Angiogenic Effect of Isoprenaline on Human Umbilical Vein Endothelial Cells via Regulation of Noncoding RNAs β-adrenoceptors play a crucial regulatory role in blood vessel endothelial cells. Isoprenaline (ISO, a β-adrenergic agonist) has been reported to promote angiogenesis through upregulation of vascular endothelial growth factor (VEGF) expression
Isoprenaline Induces Periostin Expression in Gastric Cancer Periostin mediates critical steps in gastric cancer and is involved in various signaling pathways. However, the roles of periostin in promoting gastric cancer metastasis are not clear. The aim of this study was to investigate the relevance between periostin expression and gastric cancer progression and the role of stress-related ). Furthermore, the distribution patterns of periostin were broader as the clinical staging of tumors progressed. We also identified a role of stress-related signaling in promoting cancer development and progression, and found that isoprenaline upregulated expression levels of periostin in gastric cancer cells. These findings suggest that the distribution pattern of periostin was broader as the clinical
Cardioprotective effect of total Saponins from three medicinal species of Dioscorea against isoprenaline-induced myocardial ischemia. As folk medicines used in China since 1950s, Dioscorea nipponica Makino (DN), D. panthaica Prain et Burkill (DP), and D. zingiberensis C.H. Wright (DZ) are regarded as having more or less the same traditional therapeutic actions, such as activating blood superoxide dismutases (SOD), catalase (CAT), glutathione peroxidase (GPx), the total antioxidant capacity (T-AOC), and malondialdehyde (MDA), as well as myocardial histology, were compared among rat groups administered with total saponins (TS) of DN, DP or DZ (abbreviated as DNTS, DPTS and DZTS, respectively). The rats experienced myocardial ischemia induced by isoprenaline (ISO) injection; the test
Atropine vs Isoprenaline in the Invasive Diagnosis of Arrhythmias During electrophysiological study (EPS) multiple drugs are used to reveal arrhythmias and/or conductive system disorders. Two most often used agents are atropine and isoprenaline. Due to their distinct pharmacological properties, they are affecting myocardium in different manner. Those dissimilarities can affect the EPS course and/or conductive system disorders. Two most often used are atropine and isoprenaline. Atropine is a natural, selective antagonist of cholinergic receptors M1 and M2. It reverses the inhibitory effect of vagal nerve on myocardium. This improves sinus node automatism and conduction in atrioventricular node. Isoprenaline is a preferential agonist of beta-1-adrenergic receptors. It has bathmotropic and chronotropic
Isoprenaline: A Potential Contributor in Sick Sinus Syndrome—Insights from a Mathematical Model of the Rabbit Sinoatrial Node The mechanism of isoprenaline exerting its effects on cardiac pacemaking and driving in sick sinus syndrome is controversial and unresolved. In this paper, mathematical models for rabbit sinoatrial node cells were modified by incorporating equations for the known dose -dependent actions of isoprenaline on various ionic channel currents, the intracellular Ca²⁺ transient, and i(Na) changes induced by SCN5A gene mutations; the cell models were also incorporated into an intact SAN-atrium model of the rabbit heart that is based on both heterogeneities of the SAN electrophysiology and histological structure. Our results show that, in both central and peripheral cell models
Adenylyl cyclase-mediated effects contribute to increased Isoprenaline-induced cardiac contractility in TRPM4-deficient mice. TRPM4 and TRPM5 proteins belong to the Transient Receptor Potential (TRP) ion channel family and form Ca(2+)-activated nonselective cation channels. Recently we showed a significant increase of Isoprenaline-induced inotropy in TRPM4-deficient (Trpm4(-/-)) mice to this process using TRPM4/TRPM5-double deficient (Trpm4/Trpm5((-/-)2)) mice. We performed contractility measurements on isolated papillary muscles from wild type, Trpm4(-/-) and Trpm4/Trpm5((-/-)2) mice. As shown in Trpm4(-/-) mice, Isoprenaline-induced inotropy in Trpm4/Trpm5((-/-)2) papillary muscles was significantly increased compared to wild type, whereas basal, frequency- and Ca(2+)-dependent