Estimation of IncSNHG1 Gene Expression as Potential Biomarkers of Migraine

Abstract

Background: Neuroinflammatory events and trigeminal nucleus caudalis (TNC) microglia activation play a crucial role in the pathophysiology of migraine, especially chronic migraine. The function of SIRT1 in neural tissues is anti-inflammatory and protective.

Materials and Methods: The expression level of incSNHG1, miR-181a and SIRT1 were compared between migraineur and healthy control in a case-control study, while the protein level of SIRT1 in migraineurs was compared with that of healthy controls. During the study period, patients who visited the neurology outpatient clinic were enlisted. Migraine was diagnosed by a qualified neurologist, using the criteria of the International Classification of Headache Disorders (ICHD-3).

Results: The mean relative expression of lncSNHG1 was lower in the migraine group (1.635 \pm 0.5900) as compared to the control group (2.106 \pm 0.6852). The relative levels of miR-181a expression were measured in patients versus healthy controls. Mean Expression: The patient group's mean relative expression of miR-181a was substantially greater than the control group's (1.499 \pm 0.5793, = 0.1496) (2.014 \pm 0.7233, = 0.1321). Patients' mean expression of SIRT1 was compared with the mean expression in the control group: Mean Expression: The SIRT1 group mean gene expression was 1.506 \pm 0.6091 = 0.1112, compared to the control group mean gene expression 2.106 \pm 0.6852 = 0.1769. The serum SIRT1 protein levels (ng/l) of patients and healthy controls were measured and compared. Mean Serum Levels: Compared to healthy controls (497.2 \pm 137.6 \ ng/l, = 39.73), the patient group's serum levels of SIRT1 protein were considerably lower (316.7 \pm 167.6 \ ng/l = 30.60).

To conclude, the results indicate that the alterations of lncSNHG1, miR-181a and SIRT1 may be associated with migraine, and may provide molecular markers that will aid in understanding the disease. Specifically, the reduction of SIRT1 expression in the genome and proteins indicates an involvement of impaired inflammatory and anti-inflammatory mechanisms and antioxidant activity in migraine. Larger cohorts of patients, different migraine subtypes and severity parameters, and functional molecular experiments are needed in the future to further validate the clinical relevance and mechanism of these markers.