Abstract

Clenbuterol, the β2-adrenoceptor agonist, is gaining growing popularity because of its effects on weight loss (i.e., chemical liposuction). It is also popular in bodybuilding and professional sports, due to its effects that are similar to anabolic steroids. However, it is prohibited by anti-doping control. On the other hand, it is suggested that clenbuterol can inhibit the inflammatory process. The cells from 14 untrained and 14 well-trained race horses were collected after acute exercise and cultured with clenbuterol. The expressions of CD4, CD8, FoxP3, CD14, MHCII, and CD5 in PBMC, and reactive oxygen species (ROS) production, as well as cell proliferation, were evaluated by flow cytometry. In addition, IL-1β, IL-4, IL-6, IL-10, IL-17, INF-γ and TNF-α concentrations were evaluated by ELISA. β2-adrenoceptor stimulation leads to enhanced anti-inflammatory properties in well-trained horses, as do low doses in untrained animals. In contrast, higher clenbuterol doses create a pro-inflammatory environment in inexperienced horses. In conclusion, β2-adrenoceptor stimulation leads to a biphasic response. In addition, the immune cells are more sensitive to drug abuse in inexperienced individuals under physical training.

Highlights

  • The data obtained are inversely proportional to the proliferative activity because with each cell division, the fluorescence intensity of the dye becomes lower

  • There is an increase in cortisol concentration, which is a which is a beneficial response to physical activity because it plays an essential role in adbeneficial response to physical activity because it plays an essential role in adaptation duraptation during exercise [30]

  • This study showed increased lymphocytes’ proliferation obtained from race horses under CLEN treatment

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Summary

Introduction

Publisher’s Note: MDPI stays neutral with regard to jurisdictional claims in published maps and institutional affiliations. Clenbuterol (CLEN) is a selective β2-adrenergic agonist (β2/β1 ratio = 4.0) [1]. It is lipid-soluble, and it crosses the blood–brain barrier [1,2]. The action of CLEN is caused by binding to β2-adrenoceptors (β2-ARs) and activating adenylyl cyclase

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