Migren Atağı Sırasında Serum Inflamazom Aktivasyonu Belirteçlerinin Analizi

Abstract

Pathogenesis of migraine, a significant health issue of our time, has not yet been elucidated. Cortical spreading depression (CSD), associated with migraine aura has been shown in mice to activate neuronal inflammasomes and HMGB1 release and resultant trigeminovascular activation. Considering possibility of a similar process occurring in migraine, we aimed to investigate the venous HMGB1 level during headache attack. HMGB1 level was also studied in jugular venous blood of rats after CSD. In rats, following CSD initiated via two different methods, a significant increase in jugular HMGB1 compared to basal levels was detected after one hour and this increase persisted for three hours following CSD. No significant change in HMGB1 was detected in control group. These findings are consistent with previous clinical studies showing increased levels of cytokines in internal jugular venous blood of patients during migraine. Meanwhile, in migraine patients, when compared with those samples drawn 24 hours and at least 5 days after the end of attack, no significant change in HMGB1 level was found within the first three hours of attack with or without aura. When microvesicle pools were isolated from the serum samples, HMGB1 was detected within those pools, however no significant difference was found between headache and headache-free periods. In conclusion, this study has shown that in rats following CSD, HMGB1 released from brain may be detected in central venous blood within one hour, and we were unable to demonstrate a similar increase in HMGB1 level in peripheral venous blood of patients during migraine attack. This discrepancy between experimental and clinical findings might depend on patient factors or technical issues. In the next phase, if specific analysis of HMGB1 acutely released from brain becomes available, possibly with help of microvesicle pools, it might be probable to better demonstrate the role of HMGB1 and inflammasome activation in migraine pathogenesis, leading to development of reasonable novel therapeutic approaches.