Abstract:
:Interleukin-33 (IL-33) is closely related to the regulation of immunological cells, and its receptor ST2 is a member of the interleukin-1 (IL-1) receptor family. Inflammatory responses play critical roles in neuronal damage and white matter injury (WMI) post intracerebral hemorrhage (ICH). In this study, we tried to explore the role of IL-33 in neuronal damage and WMI after ICH and the underlying mechanisms. The in vivo ICH model was performed by autologous whole blood injection into the right basal ganglia in rats. Immunoblotting, immunofluorescence, brain water content measurement, FJB staining, and TUNEL staining were applied in this study. IL-33 expression was increased in whole brain tissues post-ICH, mainly rapidly increased in ipsilateral astrocyte and microglia, but stayed at a low level in neurons. Intracerebroventricular infusion of IL-33 after ICH attenuated short-term and long-term neurological deficits, WMI, neuronal degeneration, cell death and promoted the transformation of microglia phenotype from M1 to M2 in brain tissues after ICH. These results suggest that IL-33 reduces neuronal damage and WMI by promoting microglia M2 polarization after ICH, thereby improving the outcomes of neurological function.
journal_name
Brain Res Bulljournal_title
Brain research bulletinauthors
Chen Z,Xu N,Dai X,Zhao C,Wu X,Shankar S,Huang H,Wang Zdoi
10.1016/j.brainresbull.2019.05.016subject
Has Abstractpub_date
2019-08-01 00:00:00pages
127-135eissn
0361-9230issn
1873-2747pii
S0361-9230(18)30907-9journal_volume
150pub_type
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