Evaluation of the effect of apixaban on the primary intact intervertebral disc cell cultures

Abstract

Aim: Apixaban is a frequently preferred pharmacological agent in clinics to prevent deep vein thrombosis and pulmonary embolism.Such new oral anticoagulants may cause hemorrhage’s in tissues and/or organs or may cause gastrointestinal symptoms withoutbleeding. It is also reported in the literature that it may lead to mental disorders, unwanted disorders in the urinary tract and skeletalmuscle system. However, when the literature is examined, there are no studies, which are of high-evidential value, evaluating theefficacy of apixaban on healthy, intact intervertebral disc tissue, and matrix-like structures. In this pharmaco-molecular study, itwas aimed to investigate the effects of a new oral anticoagulant agent containing the active ingredient apixaban on the intactintervertebral disc tissue cells, extracellular matrix (ECM) structure and to evaluate its positive and / or negative effects on geneexpressions of cartilage oligo matrix protein (COMP), chondroadherin (CHAD), and Matrix Metalloproteinase (MMP)s.Material and Methods: The primary cell cultures were prepared from the intact tissues of the patients with the traumatic intervertebraldisc herniation. Apixaban was administered to the cultures and molecular analyses were performed for 21 days. The data obtainedfrom the apixaban-administered and non-apixaban-administered samples were evaluated statistically and the significance valuewas accepted as P <0.05.Results: The changes were observed in the cell proliferation and the expressions of the mentioned genes in the apixabanadministered group. The suppression of COMP value and the increase in MMP-13 value may be indicative of the development ofmatrix degeneration in the apixaban-administered group, compared to the non-drug-administered control group.Conclusion: The selectivity is one of the most important features of the drugs. However, it should not be forgotten that no drug willonly produce the desired effect.