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Effects of Salidroside on gene expression in ischemic brain of rats

ABSTRACT: We employed DNA microarray to identify genes differentially regulated by salidroside in ischemic brain of MCAO rats. With a cut of p < .01 and 2-fold change, we found that 121 genes were upregulated and 142 genes were down-regulated in the MCAO group, compared to the sham group. Administration of salidroside (1 h after reperfusion, daily for 6 d) enhanced 28 transcripts and suppressed 16 transcripts. The genes involved in neuroplasticity and oxygen carrier were further confirmed by qRT-PCR. Our data suggest that salidroside could regulate neuroplasticity in post-ischemic stroke, in addition to its neuroportective function.

ORGANISM(S): Rattus norvegicus

PROVIDER: GSE52001 | GEO | 2015/10/30

SECONDARY ACCESSION(S): PRJNA226085

REPOSITORIES: GEO

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Effects of Salidroside on gene expression in ischemic brain of rats

Project description:We employed DNA microarray to identify genes differentially regulated by salidroside in ischemic brain of MCAO rats. With a cut of p < .01 and 2-fold change, we found that 121 genes were upregulated and 142 genes were down-regulated in the MCAO group, compared to the sham group. Administration of salidroside (1 h after reperfusion, daily for 6 d) enhanced 28 transcripts and suppressed 16 transcripts. The genes involved in neuroplasticity and oxygen carrier were further confirmed by qRT-PCR. Our data suggest that salidroside could regulate neuroplasticity in post-ischemic stroke, in addition to its neuroportective function. MCAO rats were injected intraperitoneally with salidroside (50 mg/kg body weight) or vehicle (saline) once a day for 6 d, commencing 1 h after reperfusion (n=3 /group). Ischemic brain was dissected for RNA extraction. Differential gene expression regulated by salidroside were analysed by microarray and subsequently confirmed by qRT-PCR.

2015-10-30 | E-GEOD-52001 | biostudies-arrayexpress

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Project description:Ischemic tolerance can be induced by numerous preconditioning stimuli, including various Toll-like receptor (TLR) ligands. We have shown previously that systemic administration of the TLR4 ligand, lipopolysaccharide (LPS) or the TLR9 ligand, unmethylated CpG ODNs prior to transient brain ischemia in mice confers substantial protection against ischemic damage. To elucidate the molecular mechanisms of preconditioning, we compared brain and blood genomic profiles in response to preconditioning with these TLR ligands and to preconditioning via exposure to brief ischemia. The experiment is a comparison of multiple treatment groups with sampling at multiple time points. The objective is to identify differentially regulated genes associated with preconditioning. Time points are examined both following preconditioning alone and following subsequent ischemic challenge (middle cerebral artery occlusion (MCAO)). Brain ipsilateral cortex tissue and blood were collected and processed from each animal. 6 experimental conditions: (n=3-4 mice/condition) LPS treated (i.p. 0.2mg/kg) + ischemic challenge (45min MCAO) CpG treated (i.p. 0.8mg/kg) + ischemic challenge (45min MCAO) Saline treated (i.p.) + ischemic challenge (45min MCAO) brief ischemia (12 min MCAO) + ischemic challenge (45min MCAO) Sham of brief ischemia (12 min) + ischemic challenge (45min MCAO) Non-treated + ischemic challenge (45min MCAO) Time points: Pre-ischemic challenge 3hr 24hr 72hr Post-ischemic challenge 3hr 24hr Unhandled (6 mice)-BASELINE

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Project description:To further delineate tPA functions in the blood, we examined the gene expression profiles induced by tPA in a rat model of ischemic stroke. Forty-two Sprague-Dawley rats were subjected to: 2 hours of middle cerebral artery occlusion (MCAO); a permanent-MCAO; or were used as controls. tPA was administered to half of the rats in each group at 3hours. Whole blood was drawn at 24 hours, and isolated RNA levels measured on Affymetrix Rat Genome 230 2.0 GeneChip microarrays to examine the entire RNA transcriptome. 42 samples, 7 groups in total ( 2 treatmented disease, 2 untreated disease, and 3 control groups), each group had 6 replicates

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Transcriptome analysis reveals intermittent fasting-induced genetic changes in ischemic stroke

Project description:Intermittent fasting is previously reported to exhibit neuroprotection against experimental ischemic stroke. However, the detailed understanding of protection mechanisms are lacking. By observing the overall transcriptomic changes in each timepoint of ischemic stroke would benefit the understanding of underlying active pathways and mechanisms. Here, we conduct experimental MCAO ischemic stroke on mice exposed to different daily intermittent fasting method to compare not only among the ischemic stroke timepoints but also the efficacy of different intermittent fasting interventions. Our current study presented the transcriptomic changes for the first time in specific timepoints of ischemic stroke as well as under the condition of intermittent fasting. A number of neuroprotective mechanisms-related genes were significantly affected by intermittent fasting conditions in differential manners.

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Proteomic analysis of the aggregated proteins in cerebral vessles from MYPT1SMKO mice

Project description:To comprehensively understand the mechanism by which MYPT1 modulates the phenotypic switching of VSMCs after ischemic stroke, the proteins of cortical small vessel from MYPT1SMKO and WT mice subjected to MCAO or sham group were collected for proteomic screening.

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Mouse ischemic tolerance genomic analysis of the brain and blood.

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