Fig 1.
1H spectrum of the ipsilateral thalamus.
Acquired 1H spectrum of the ipsilateral thalamus of an animal exposed to HI. Cr, creatine; DMSO, dimethyl sulfoxide; Gln, glutamine; Glu, glutamate; GPC, glycerophosphocholine; GSH, glutathione; Ins, myo-inositol; NAA, N-acetyl aspartate; PCh, phosphocoline; PCr, phosphocreatine; Tau, taurine.
Fig 2.
Metabolic profiles of the ipsilateral thalamus of HI and sham animals 1 day after HI.
(a) The PCA score plot shows the metabolic profiles of all animals. The HI animals were separated from the sham animals with the corresponding loading plot of PC 1 (b) showing the metabolic alterations that caused this separation. The shaded area is drawn based on visual inspection and is meant to highlight the separation between the groups. Glx, glutamine+glutamate; GPC glycerophosphocholine; HI, hypoxia-ischemia; NAA, N-acetyl aspartate; NAAG, N-acetyl aspartyl glutamate; MM, macromolecules; Lip, lipids; PC, principle component; PCA, principle component analysis; PCh, phosphocholine; PCr, phosphocreatine; ppm, parts per million.
Fig 3.
Metabolite concentrations in the ipsilateral thalamus within 1 day after HI.
Concentrations of (a) energy metabolites, (b) neurotransmitters, (c) anti-oxidants and osmolytes, (d) metabolites representing cell injury/viability and (e) lipids and macromolecules in HI animals exposed to PBS, DMSO or melatonin (MEL) treatment and sham animals (here presented as one group). Results are presented as mean ± SEM. * significant differences between groups. GPC glycerophosphocholine; HI, hypoxia-ischemia; Lip, lipids; MM, macromolecules; NAA, N-acetyl aspartate; ppm, parts per million; sham, sham-operated.
Fig 4.
Metabolic profiles of the ipsilateral thalamus of HI animals after 2 treatment injections.
(a) The metabolic profiles of the HI animals treated with either melatonin (10 mg/kg) dissolved in PBS with 5% DMSO (MEL), PBS with 5% DMSO (DMSO) or only PBS (PBS) are displayed in the PCA score plot. The shaded area marks the animals treated with melatonin with higher levels of energy metabolites, neurotransmitters and macromolecules as shown in (b). (b) The corresponding loading plot shows the metabolic alterations related to the separation along PC 1. Glx, glutamine+glutamate; GPC glycerophosphocholine; HI, hypoxia-ischemia; NAA, N-acetyl aspartate; NAAG, N-acetyl aspartyl glutamate; MM, macromolecules; Lip, lipids; PC, principle component; PCA, principle component analysis; PCh, phosphocholine; PCr, phosphocreatine; ppm, parts per million.
Fig 5.
Metabolite concentrations in the contralateral thalamus within 1 day after HI.
Concentrations of (a) energy metabolites, (b) neurotransmitters, (c) anti-oxidants and osmolytes, (d) metabolites representing cell injury/viability and (e) lipids and macromolecules in HI animals exposed to PBS, DMSO or melatonin (MEL) treatment and sham animals (here presented as one group). Results are presented as mean ± SEM. * significant differences between groups. GPC glycerophosphocholine; HI, hypoxia-ischemia; Lip, lipids; MM, macromolecules; NAA, N-acetyl aspartate; ppm, parts per million; sham, sham-operated.