Cortical Expression Of SOCS3 After Experimental Subarachnoid Hemorrhage Model In Rats

Objective Subarachnoid hemorrhage (SAH) is a kind of serious neurosurgical diseases. Early brain injury (EBI) after SAH plays an important role in the development of delayed ischemia, and it is a primary cause of morbidity and mortality in patients with SAH. Oxidative stress, immune pathophysiology of inflammation, apoptosis and other changes could be found after SAH. JAK/STAT signaling pathway is involved in multiple signaling pathways involved in cascades, cytokine signal transduction negative regulatory factor 3 (SOCS3) through the JAK/STAT signaling pathway. Thus considering early brain injury after subarachnoid hemorrhage, SOCS3 participates in its physiological and pathological processes, and to play the role of regulating signal transduction. This experiment is to study the expression and distribution of suppressor of cytokine signaling 3 (SOCS3) in the brain after experimental SAH in rats. Methods A total of 72 male SD rats were randomly divided into nine groups:control group, SAH 6h,12h,24h,48h,72h,5d and 7d groups. The animals in SAH 6h,12h,24h,48h,72h,5d and 7d groups were subjected to experimental SAH, and then were killed at corresponding time points after blood injection, respectively (n=8 for each group). Western-blot analysis and immunohistochemical study were performed to evaluate the expression of SOCS3 in the brain after SAH. RT-PCR analysis was used to detect the proinflammatory cytokines IL-1β and TNF-a expression.Results The protein levels of SOCS3was significantly elevated after SAH, with a peak at 24h after SAH, and then decreased gradually. In addition, SOCS3 was mainly located in the cytosol in control group, while it significantly increased in the cytosol when activated after SAH. At 24h after SAH, the cytosol of SOCS3 immunoreactivity was peaked and then SOCS3 immunoreactivty decreased in both cytosol and nuclei. RT-PCR shows a significant increase in the expression of inflammatory mediators IL-1β. Itbegan to increase after 3h, with two peaks at Id and 5d, respectively. TNF-a peaked at 3h, and then gradually decrease.Conclusion socs3 activation exists in the early period after experimental SAH in rats, suggesting that socs3 activation involved in the pathophysiology of early brain injury after SAH. Inflammatory cytokines IL-1β and TNF-a SAH are involved in physiological and pathological processes, possibly playing a key role in EBI after SAH through SOCS3.