Ischemic stroke, a devastating disease with a complex pathophysiology, is a leading cause of death and disability worldwide. In our previous study, we reported that
galangin provided direct protection against ischemic injury and acted as a potential
neuroprotective agent. However, its associated neuroprotective mechanism has not yet been clarified. In this paper, we explored the potential AA
biomarkers in the acute phase of
cerebral ischemia and the effect of
galangin on those potential
biomarkers. In our study, 12 AAs were quantified in rat serum and found to be impaired by
middle cerebral artery occlusion (MCAO)-induced focal
cerebral ischemia. Using partial least squares discriminate analysis (PLS-DA), we identified the following
amino acids as potential
biomarkers of
cerebral ischemia:
glutamic acid (Glu),
homocysteine (Hcy),
methionine (Met),
tryptophan (Trp),
aspartic acid (Asp),
alanine (Ala) and
tyrosine (Tyr). Moreover, four
amino acids (Hcy,
Met, Glu and Trp) showed significant change in
galangin-treated (100 and 50 mg kg(-1)) groups compared to vehicle groups. Furthermore, we identified three pathway-related
enzymes tyrosine aminotransferase (TAT),
glutamine synthetase (GLUL) and monocarboxylate transporter (SLC16A10) by multiplex interactions with Glu and Hcy, which have been previously reported to be closely related to
cerebral ischemia. Through an analysis of the metabolite-
protein network analysis, we identified 16
proteins that were associated with two
amino acids by multiple interactions with three
enzymes; five of them may become potential
biomarkers of
galangin for
acute ischemic stroke as the result of molecule docking. Our results may help develop novel strategies to explore the mechanism of
cerebral ischemia, discover potential targets for
drug candidates and elucidate the related regulatory signal network.