In vivo administration of acepromazine or promethazine to horse decreases the reactive oxygen species production response of subsequently isolated neutrophils to stimulation with phorbol myristate acetate.
- Journal Article
Summary
This research explores the impact of two drugs, acepromazine and promethazine, on the production of reactive oxygen species (ROS) in a horse’s neutrophils and suggests these drugs could potentially be beneficial for horses with inflammatory diseases.
Understanding the Research
This research is focused on the exploration of two types of phenothiazines – acepromazine and promethazine – and their influence on the production of reactive oxygen species (ROS) in horses.
- Phenothiazines are a group of drugs that have been known to exhibit antioxidant and anti-inflammatory properties in previous in-vitro studies. In this study, the researchers decided to examine these properties in a live organism, hence the “in vivo” experimentation.
- Reactive Oxygen Species (ROS) are chemically reactive molecules containing oxygen that play a vital role in cell signalling and inflammation. However, excessive ROS can lead to cellular damage, hence triggering an inflammatory response.
- Neutrophils are a type of white blood cell critical to an organism’s immune response system. They are often the first cells to respond to inflammation and produce ROS as part of their defensive strategy.
Methodology and Results
This study used two batches of horses, administering an intravenous dose of 0.1 mg/kg of either acepromazine or promethazine.
- Blood samples from these animals were collected five times: once before the drug administration (T0), and again 0.5, 1, 3, and 5 hours after administration.
- The researchers analysed the blood samples, measuring the chemiluminescence (CML) response of the neutrophils ex vivo. In other words, they observed the light produced during the neutrophils’ reactive response in the presence of a substance called luminol.
- The maximum chemiluminescence value (peak value) was recorded for each sample.
- The results indicated a significant reduction in ROS production in the group treated with acepromazine and promethazine. Specifically, a 49% reduction was observed at 5 hours after administration in the acepromazine group, and a 24% reduction at 3 hours after administration in the promethazine group.
Implications of the Study
The research findings are important because they show that acepromazine and promethazine may have a therapeutic effect on horses with inflammatory diseases.
- In inflammatory conditions, neutrophils are activated and produce ROS, contributing to the inflammatory response. Therefore, a reduction in ROS production could help to manage these conditions.
- The potency of these drugs in reducing ROS production in horse neutrophils indicates that they could be used as anti-inflammatory treatments in equine medicine.
Cite This Article
Publication
Researcher Affiliations
- University of Liège, Faculty of Veterinary Medicine, Equine Clinic, B41, 4000 Liège 1, Belgium.
MeSH Terms
- Acepromazine / administration & dosage
- Acepromazine / pharmacology
- Animals
- Antioxidants / pharmacology
- Cells, Cultured
- Dopamine Antagonists / pharmacology
- Horses
- Neutrophils / drug effects
- Neutrophils / metabolism
- Promethazine / administration & dosage
- Promethazine / pharmacology
- Reactive Oxygen Species / metabolism
- Tetradecanoylphorbol Acetate / pharmacology
Citations
This article has been cited 3 times.- Kandeel M, Almubarak AI, Hussen J, El-Deeb W, Venugopala KN. Pharmacokinetic, Clinical, and Myeloid Marker Responses to Acepromazine Sedation in Arabian Camels.. Front Vet Sci 2021;8:725841.
- Smith MR, Glicksberg BS, Li L, Chen R, Morishita H, Dudley JT. Loss-of-function of neuroplasticity-related genes confers risk for human neurodevelopmental disorders.. Pac Symp Biocomput 2018;23:68-79.
- Pequito M, Amory H, de Moffarts B, Busoni V, Serteyn D, Sandersen C. Evaluation of acepromazine-induced hemodynamic alterations and reversal with norepinephrine infusion in standing horses.. Can Vet J 2013 Feb;54(2):150-6.