Due to sudden loss of cerebral blood circulation,
acute ischemic stroke (IS) causes neuronal energy attenuation or even exhaustion by
mitochondrial dysfunction resulting in aggravation of neurological injury. In this study, we investigated if
Notoginsenoside R1 ameliorated cerebral energy metabolism by limiting neuronal
mitochondrial dysfunction in acute IS. Male Sprague-Dawley rats (260-280 g) were selected and performed by permanent
middle cerebral artery occlusion model. In vitro, the
oxygen glucose deprivation (OGD) model of Neuro2a (N2a) cells was established. We found
Notoginsenoside R1 treatment reduced rats'
cerebral infarct volume and neurological deficits, with increased
Adenosine triphosphate (
ATP) level together with upregulated expression of
glucose transporter 1/3, monocarboxylate transporter 1 and
citrate synthase in brain peri-ischemic tissue. In vitro, OGD-induced N2a cell death was inhibited, cell mitochondrial morphology was improved. Mitochondrial amount, mitochondrial membrane potential, and
mitochondrial DNA copy number were increased by
Notoginsenoside R1 administration. Furthermore, mitochondrial energy metabolism-related
mRNA array found Atp12a and Atp6v1g3 gene expression were upregulated more than twofold, which were also verified in rat ischemic tissue by quantitative polymerase chain reaction (qPCR) assay. Therefore,
Notoginsenoside R1 administration increases cerebral
glucose and
lactate transportation and
ATP levels, ameliorates neuronal mitochondrial function after IS.
Notoginsenoside R1 may be a novel
protective agent for neuronal mitochondria poststroke.