相关实验视频
Updated: Jun 6, 2026

07:26
Isolation of Functional Cardiac Immune Cells
Published on: December 5, 2011
慢性β-上腺刺激诱导心肌前炎性细胞因子表达
D R Murray1, S D Prabhu, B Chandrasekar
1Department of Medicine/Cardiology, University of Texas Health Science Center at San Antonio, South Texas Veterans Healthcare System-Audie Murphy Division, San Antonio, Texas, USA. murrayd@uthscsa.edu
Circulation
|May 24, 2000
概括
在老鼠中,慢性β-上腺刺激会增加心肌细胞因子瘤缩因子-α (TNF-α),联素-1β (IL-1β) 和IL-6. 这种效应局限于心脏组织,不存在于全身循环中.
科学领域:
- 心血管生理学心血管生理学
- 神经免疫学 神经免疫学
- 分子生物学分子生物学
背景情况:
- 充血性心力衰竭的病理生理学涉及同情神经系统和促炎细胞因子.
- 这些神经激素系统之间的关系需要进一步研究.
研究的目的:
- 调查慢性β-上腺刺激对心肌和瘤亡因子-α (TNF-alpha),互白素-1β (IL-1β) 和IL-6的系统性阐述的影响.
主要方法:
- 雄性大鼠被用L-异二醇或盐水治疗了7天.
- 肌肉细胞因子表达 (mRNA和蛋白质) 用北方涂抹,西方涂抹和免疫组织化学分析.
- 循环中的细胞因子水平用ELISA测量.
主要成果:
- L-异二醇显著增加了心肌的mRNA和TNF-alpha,IL-1beta和IL-6的蛋白质表达.
- 免疫组织化学证实了这些细胞因子在被治疗的老鼠的心肌内存在.
- 在任何治疗组的血清中都没有发现这些细胞因子的可检测水平.
结论:
- 慢性β-上腺刺激会在心肌内诱导TNF-alpha,IL-1beta和IL-6的提升.
- 这种效应局限于心脏,不会导致这些细胞因子的全身升高.
相关概念视频
Adrenergic Receptors: β Subtype
β-adrenoceptors have varied sensitivities towards adrenaline, noradrenaline, and isoprenaline. The order of agonist potency is as follows:
Isoprenaline > Adrenaline > Noradrenaline
Neurotransmitter binding to these receptors causes activation of adenylyl cyclase resulting in increased concentrations of cAMP and modulation of calcium ion channels within the cell. They are further classified into β1, β2, and β3 subtypes.
β1-adrenoceptors: β1-adrenoceptors have equal affinities for...
Isoprenaline > Adrenaline > Noradrenaline
Neurotransmitter binding to these receptors causes activation of adenylyl cyclase resulting in increased concentrations of cAMP and modulation of calcium ion channels within the cell. They are further classified into β1, β2, and β3 subtypes.
β1-adrenoceptors: β1-adrenoceptors have equal affinities for...
Antihypertensive Drugs: Action of β1 Blockers
β1-receptors are primarily located in the heart and kidneys. In cardiac myocytes, these receptors interact with neurotransmitters released by the sympathetic nervous system during heightened activity or danger. As a result, β1-receptors get activated, initiating a series of biochemical processes. Excessive activation of beta receptors due to chronic stress can abnormally increase heart rate and contractility, resulting in high blood pressure or hypertension. To counteract this, β1-blockers...
Myocarditis I: Introduction
Myocarditis is inflammation of the myocardium, which is the muscular layer of the heart.EtiologyMyocarditis has a diverse etiology, including a wide range of infectious and non-infectious causes:Infectious CausesViral: Common viruses include Coxsackie A and B, adenovirus, parvovirus B19, enteroviruses, and influenza A.Bacterial: Examples include infections caused by Streptococcus, Staphylococcus, and Mycoplasma species.Rickettsial: Infections like Rocky Mountain spotted fever can result in...
Myocarditis II: Clinical Features and Diagnostic Tests
Myocarditis is an inflammation of the heart muscle. The symptoms vary widely, encompassing asymptomatic presentations to severe, acute manifestations.Clinical PresentationAsymptomatic cases: In some instances, myocarditis may be asymptomatic, with the infection resolving without intervention. These cases often go undetected unless discovered incidentally through diagnostic imaging or tests conducted for other reasons.General Early Symptoms: Early symptoms of myocarditis are non-specific and can...
Myocarditis III: Medical Management
Myocarditis: Comprehensive Medical ManagementMyocarditis, the heart muscle inflammation, requires a comprehensive medical management strategy that addresses the underlying cause, provides supportive care, manages symptoms, and reduces cardiac workload.Infections and Autoimmune CausesAdminister appropriate antimicrobial therapy when an infectious agent causes myocarditis. For instance, penicillin treats infections caused by Group A Streptococcus. In cases where autoimmune processes are...
Chronic Inflammation: Introduction
Chronic inflammation is a prolonged, dysregulated immune response that persists for weeks to years when the inciting stimulus is difficult to eradicate or when self‑antigens drive ongoing reactivity. Morphologically, it is defined by mononuclear cell infiltration, progressive tissue destruction, and concurrent attempts at healing via angiogenesis and fibrosis. Compared with acute inflammation, edema is less prominent while cellular infiltration predominates; triggers include persistent...

