相关实验视频
Updated: May 5, 2026
11:02
Isolation and Physiological Analysis of Mouse Cardiomyocytes
Published on: September 7, 2014
22.9K
室腔肌细胞位直接负责内毒素诱导的心脏功能障碍
Steve Lancel1, Olivier Joulin, Raphael Favory
1EA 2689, CHRU, and Université de Lille 2, IFR 114 IMPRT, Lille, France.
Circulation
|May 18, 2005
概括
败血症通过激活左心室 (LV) 心肌细胞中的卡斯帕斯引起心脏功能障碍,导致收缩性降低和瘤损伤. 用zVAD.fmk抑制卡斯帕斯可以在败血症模型中防止这些有害影响.
科学领域:
- 心脏病学 心脏病学
- 分子生物学分子生物学
- 细胞生物学 细胞生物学
背景情况:
- 败血症诱导的亡通常与淋巴细胞死亡有关.
- 酶激活可能直接损害器官系统细胞功能.
- 这项研究调查了在败血症期间左心室 (LV) 心肌细胞中卡斯帕斯激活.
研究的目的:
- 确定左心室 (LV) 心肌细胞卡斯帕酶激活是否直接导致败血症引起的心脏收缩功能障碍.
- 在细胞水平上探索将败血症与心脏功能障碍联系起来的分子机制.
主要方法:
- 从注射了内毒素的老鼠中分离的LV心肌细胞被分析了收缩功能和卡斯帕斯活性.
- 使用西式涂抹和酶定量测试来评估酶激活和肌纤维裂变.
- 使用zVAD.fmk和zDEVD.cmk抑制caspases被用于体内和体外.
主要成果:
- 在老鼠中注射内毒素导致LV心肌细胞收缩储量减少和肌纤维对的反应.
- 在LV心肌细胞中观察到酶-3, -8和 -9类活性增加,与瘤细胞破坏和托罗邦素T裂变相关.
- 用zVAD.fmk治疗预防了败血症诱导的LV心肌细胞功能障碍,瘤损伤和托罗邦素T裂变.
- 接受内毒素治疗的老鼠血清诱导了原始心肌细胞的收缩功能障碍和卡斯巴酶激活,卡斯巴酶抑制剂阻断了这些效应.
结论:
- 在内毒素诱导的酶激活和LV心肌细胞中受损的收缩储备之间存在显著的联系.
- 卡斯巴酶激活直接导致沙科梅尔乱和与败血症相关的心脏功能障碍的功能性下降.
相关概念视频
01:24Caspases
8.7K
Caspase, a family of cysteine proteases, serve as effectors in apoptosis. The ced3 gene in C.elegans was first identified to be involved in apoptosis. This gene encodes the ced-3 caspase that is similar to the interleukin-1-beta converting enzyme or ICE in mammals. In addition to apoptosis, caspases also function in the inflammatory response. Inflammatory caspases are essential in activating pro-inflammatory cytokines that recruit immune cells and block the replication of pathogens inside...
8.7K
01:17The Extrinsic Apoptotic Pathway
6.2K
The extrinsic apoptotic pathway is initiated when extracellular death-inducing signals, such as specific cytokines, activate the death receptors expressed on the cell surface. The immune cells involved in this pathway are natural killer cells (NK cells) and cytotoxic T-lymphocytes. NK cells are critical in innate immune response, while cytotoxic T-lymphocytes are associated with adaptive immune response. These cells recognize specific receptors expressed on the altered cells and activate...
6.2K
01:17Pathophysiology of Heart Failure
5.1K
Heart failure (HF) is a progressive syndrome involving ventricles that leads to inadequate cardiac output. It can be classified based on location and output or ejection fraction. Ejection fraction (EF) is an essential measurement in the diagnosis and surveillance of HF. Reduced EF corresponds to systolic heart failure (HFrEF). However, HF with preserved ejection fraction (HFpEF) is becoming increasingly prevalent. Also known as diastolic HF, this form of HF is related to aging. The...
5.1K
01:21Myocarditis I: Introduction
647
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...
647
01:00Cellular Injury I: Introduction
95
Cellular injury occurs when a cell cannot maintain homeostasis or adapt to stressors such as hypoxia, toxins, or trauma. Depending on severity and duration, injury may be reversible, allowing recovery, or irreversible, leading to cell death.General Mechanisms of Cell InjuryAlthough causes vary, most cellular injuries arise from a few key mechanisms that disrupt essential functions and often amplify one another. Cell survival depends on the extent and balance of these disturbances.ATP depletion...
95
01:16Cellular Injury IV: Necrosis
97
Necrosis is a form of irreversible cell death caused by severe injury such as ischemia, toxins, or trauma. Unlike programmed cell death, it is an uncontrolled, pathological process that typically provokes inflammation in surrounding tissues.Pathophysiologic ChangesNecrosis begins when cells sustain critical damage, leading to swelling of organelles, particularly mitochondria, and rapid ATP depletion. As energy levels decline, membrane ion pumps fail, leading to calcium influx and eventually,...
97