Montelukast protects H9c2 cardiomyocytes against radiation-induced toxicity

Abstract

IntroductionRadiation-induced cardiotoxicity is a major concern following radiation treatment or involuntary radiation exposure. The normal functionality of cardiomyocytes becomes limited, which results in deleterious consequences, including an increase in the secretion of proinflammatory factors, such as HMGB1, and oxidative stress due to increased production of NOX4 and ROS. Radiation exposure results in disruption of the Bax/Bcl-2 ratio, increased expression of cytochrome c, and increased cleavage of caspase 3, thereby promoting cardiotoxicity and excessive apoptosis of cardiomyocytes. The cysLT1R antagonist montelukast is commonly used in the treatment of asthma, with recent studies showing potential for this drug in treating other diseases.Material and methodsRat H9c2 cardiomyocytes were used in all the vitro experiments. The MTT assay was used to determined the The Cell viability; DCFH-DA staning was used to measure the intracellular ROS; and TMRM method was used to determine the level of ΔΨm in H9c2 cells; All mRNA levels of gene were measured by real time-PCRResultsIn this study, we find that montelukast can mitigate the increase in oxidative stress and HMGB1 secretion induced by radiation, but also that montelukast exerts significant protective effects in terms of cell viability and apoptosis.ConclusionsThe authors of the present work hope to aid in the elucidation of the role of montelukast as a pretreatment for radiation and find safe and effective solutions to this common side effect of such a prevalent treatment in today’s society.