, Driving the Microglial Polarization, Has a Sensitivity Profile After Subarachnoid Hemorrhage.

Increasing evidence suggests that triggering receptor expressed on myeloid cells 2 () is implicated in the pathophysiology of neuroinflammation. The aim here was to investigate the neuroprotective role of and its regulatory mechanism after subarachnoid hemorrhage (SAH). siRNA was administered to measure the detrimental role of in mediating microglial polarization and after experimental SAH. The relationship between Toll-like receptor 4 () signaling and was further explored. The soluble from the cerebrospinal fluid (CSF) of patients with SAH was detected. The results showed that mainly located in the microglia and presented a markedly delayed elevation after SAH. knockdown triggered increased pro-inflammatory productions, aggravated microglial activities, and further exacerbated neurological dysfunction after SAH. Significantly, knockout increased the expression of , accompanied by ameliorated neuroinflammation and improved neurological function. Corresponding to different clinical Hunt-Hess grades, obviously enhanced accumulation of soluble was detected in the CSF of patients with SAH. played a pivotal role in mediating microglial polarization after SAH, and the neuroprotective effect of might be potentially suppressed by the hyperactive in the early phase of SAH. Pharmacological targeting of may be a promising strategy for SAH therapy.