- Academic Editor
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Background: The purpose of this study was to
investigate the potential involvement of pyruvate kinase M2 (PKM2), an enzyme
acting as a rate-limiting enzyme in the final phase of glycolysis, in the
regulation of glial activation and brain damage of intracerebral hemorrhage
(ICH). Methods: Western blotting and immunofluorescence were
performed to investigate PKM2 expression, terminal deoxynucleotidyl transferase
deoxyurinary triphosphate (dUTP) nick end labeling staining, hematoxylin and
eosin staining, and behavioral tests were employed to evaluate the brain damage
of ICH mice, and RNA-seq and bioinformatic analyses were performed to detect gene
expression changes in ICH mice treated with TEPP-46. Results: Increased
PKM2 levels in perihematomal brain tissue were found starting from 3 days
following ICH and peaked at 5 and 7 days post ICH. The increased expression of
PKM2 was mainly co-localized with glial fibrillary acidic
protein (GFAP)