The effects of interferon beta 1-alpha administration on gene expression profile of nicotinic receptors in relapsing remitting multiple sclerosis (RRMS) patients

Abstract

Multiple sclerosis (MS) is the primary cause of non-traumatic neurological impairment in young adults. It is a demyelinating disease that results in the loss of structure or function of cells in the central nervous system. A multimodal approach is necessary for the effective care of this condition in order to reduce acute attacks and manage and rectify annoying or disabling symptoms. The prognosis for many MS patients has improved significantly as a result of significant advancements in the disease's management, particularly for relapsing MS. Most often, interferon-beta 1a is used to treat multiple sclerosis. The neuromuscular junction's nicotinic acetylcholine receptor is a neurotransmitter-gated ion channel that has evolved to be as efficient and quick as possible at converting chemical signals to electrical ones. These receptors are involved in immune system modulation. These receptors are involved in the control of inflammatory and immunological responses. The purpose of this research is to look into how the interferon-beta 1a drug affects the nicotinic receptor gene expression profile in patients suffering relapsing-remitting multiple sclerosis. Methods: The PBMCs were extracted using Ficoll. Following the separation of PBMCs, cDNA was produced from the cDNA synthesis kit and cellular RNA was extracted using Trizol. Then, variations in the expression profiles of various genes belonging to various nicotinic receptors, including the beta two, alpha nine, and alpha ten subunits, were evaluated using quantitative real-time PCR. Findings: The results of the study demonstrated that, when comparing the mRNA expression of the beta two and alpha nine subunits of the nicotinic receptor across samples from healthy individuals and those with MS, there is no significant difference. On the other hand, compared to healthy individuals, MS patients exhibit a considerable decrease in the mRNA expression of nicotinic receptor alpha subunit 10. Furthermore, compared to patients who did not receive the medicine, individuals who got interferon-beta 1a showed a significant drop in the level of expression of beta-2, alpha-9, and alpha-10 subunit genes.