Abstract: Objective To explore the changes of interleukin -17A(IL-17A)in cerebrospinal fluid(CSF) and serum after ischemic stroke. And then investigate its role in ischemic neuronal injury and its possible pathway. Methods Establish mouse cerebral artery occlusion (MCAO) model and oxygen-glucose deprivation (OGD) model with cortical primary neurons, and use enzyme-linked immunosorbent assay (ELISA) to detect the level of IL-17A in serum and cerebrospinal fluid at 6, 12 h, 1, 3, 7 d and per-infarct cortex homogenates at 12 h. With 5, 10, 100 and 500 ng / mL of recombinant IL-17A (rIL-17A) and OGD treatment on wild-type mice (n = 8) and without rIL-17A treatment on knockout mice (n = 5), use MTS assay and Western Blot to detect its effect on ischemic neurons. Results IL-17A significately increased in per-infarct cortex homogenates(P<0.001, n=5) and CSF at 12 h after MCAO (P<0.05, n=5), while in serum it began to increase at 1 d(P<0.05, n=5) and peaked at 3 d (P<0.001, n=7); In vitro, rIL-17A aggravated neuronal death in dose-dependent manner after OGD while it had no effect on neuronal death under normoxia culture(P<0.05，n=8); The ratio of Cl/pro-caspase 3 and the Beclin 1 protein levels increased after OGD treatment. However, this effect could be reversed in lacking of IL-17A after OGD treatment (P<0.05, n=5). Conclusion IL-17A in the serum and CSF after ischemic stroke show different change, and it plays an important role in aggravating neuronal injury possibly through autophagy and apoptosis pathways.

Key words: Interleukin-17A, Ischemic stroke, Serum, Cerebrospinal fluid (CSF), Oxygen-glucose deprivation (OGD), Mice