Clenbuterol (hydrochloride) is a β2-adrenergic receptor agonist with an EC50 of 31.9nM[1]. Clenbuterol (hydrochloride) effectively inhibits the release of TNF-α and IL-1β induced by lipopolysaccharide (LPS)[2].
The number of CD4+ FoxP3+ T regulatory cells increased after Clenbuterol (hydrochloride) treatment (0.6ng/mL) of PBMCs, But the number of CD8+ FoxP3+ T regulatory cells remained at the untreated level[2]. Clenbuterol (hydrochloride) (10-200µM) induces cell cycle arrest in C2C12 myoblasts by delaying p27 degradation through β-arrestin 2 signaling[3]. Clenbuterol (hydrochloride) (0.01-300μM) reduced sarcomere lengt and Ca2+ transients amplitude in a concentration-dependent manner in rat cardiomyocytes (CMs) [4].
Clenbuterol (hydrochloride) (2mg/kg)-induced cardiac hypertrophy in rats mainly manifested as physiological hypertrophy, in which the left ventricular function, morphology, collagen concentration, and mRNA expression of SERCA2a and PLB in rats were normal[5]. Clenbuterol (hydrochloride) (1µmol/L; 60min) ameliorated ventricular diastolic function by enhaning Ca2+-ATPase activity and reduced oxidative stress and cardiac myocyte apoptosis in an experimental rat model of myocardium Ischaemia-Reperfusion injury[6].
References:
[1] Clenbuterol induces cell cycle arrest in C2C12 myoblasts by delaying p27 degradation through β-arrestin 2 signaling.
[2] Witkowska-Piłaszewicz O, Pingwara R, Szczepaniak J, et al. The Effect of the Clenbuterol—β2-Adrenergic Receptor Agonist on the Peripheral Blood Mononuclear Cells Proliferation, Phenotype, Functions, and Reactive Oxygen Species Production in Race Horses In Vitro[J]. Cells, 2021, 10(4): 936.
[3]. Chen M, Liu C, Wang M, et al. Clenbuterol induces cell cycle arrest in C2C12 myoblasts by delaying p27 degradation through β-arrestin 2 signaling[J]. International Journal of Biological Sciences, 2017, 13(10): 1341.
[4]. Siedlecka U, Arora M, Kolettis T, et al. Effects of clenbuterol on contractility and Ca2+ homeostasis of isolated rat ventricular myocytes[J]. American Journal of Physiology-Heart and Circulatory Physiology, 2008, 295(5): H1917-H1926.
[5]. Wong K, Boheler K R, Bishop J, et al. Clenbuterol induces cardiac hypertrophy with normal functional, morphological and molecular features[J]. Cardiovascular research, 1998, 37(1): 115-122.
[6]. Liu P, XIANG J, Zhao L, et al. Effect of β2‐adrenergic agonist clenbuterol on ischemia/reperfusion injury in isolated rat hearts and cardiomyocyte apoptosis induced by hydrogen peroxide[J]. Acta Pharmacologica Sinica, 2008, 29(6): 661-669.
Clenbuterol (hydrochloride)是一种β2-肾上腺素受体激动剂，EC50为31.9nM[1]。Clenbuterol (hydrochloride)可有效抑制脂多糖（LPS）诱导的TNF-α和IL-1β释放[2]。
用Clenbuterol (hydrochloride)（0.6ng/mL）处理PBMC后，CD4+ FoxP3+ T 调节细胞的数量增加，但CD8+ FoxP3+ T 调节细胞的数量仍保持在未处理的水平[2]。Clenbuterol (hydrochloride) （10-200µM）通过β-arrestin 2信号传导延迟p27降解，从而诱导C2C12成肌细胞中的细胞周期停滞[3]。Clenbuterol (hydrochloride) （0.01-300μM）以浓度依赖性方式降低大鼠心肌细胞（CM）的肌节长度和Ca2+瞬变幅度[4]。
Clenbuterol (hydrochloride) （2mg/kg）诱导的大鼠心脏肥大主要表现为生理性肥大，其中大鼠左心室功能、形态、胶原浓度以及SERCA2a和PLB的mRNA表达正常[5]。Clenbuterol (hydrochloride) （1µmol/L; 60min）通过增强Ca2+-ATPase活性改善心室舒张功能，并在实验性大鼠心肌缺血再灌注模型中降低氧化应激和心肌细胞凋亡[6]。