Gastrodin ameliorates the lipopolysaccharide-induced neuroinflammation in mice by downregulating miR-107-3p
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ABSTRACT:
PROVIDER: PRJNA887722 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR21823507.fastq.gz | Fastqsanger.gz | |||
| SRR21823508.fastq.gz | Fastqsanger.gz | |||
| SRR21823509.fastq.gz | Fastqsanger.gz | |||
| SRR21823510.fastq.gz | Fastqsanger.gz | |||
| SRR21823511.fastq.gz | Fastqsanger.gz |
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Project description:Background: Neuroinflammation plays a pivotal role in the pathogenesis of Central Nervous System (CNS) diseases. The phenolic glucoside gastrodin (GAS), has been known to treat CNS disorders by exerting anti-inflammatory activities. Our aim was to investigate the potential neuroprotective mechanisms of GAS on lipopolysaccharide (LPS)-induced mice. Methods: Male C57BL/6J mice were treated by LPS, before which GAS was adminisrated. The behavior tests such as forced swim test, tail suspension test, and elevated plus maze were performed to evaluate depressive-anxiety-like behaviors. A high-throughput sequencing (HTS) analysis was performed to screen out distinctive miRNAs which were validated using quantitative real-time PCR. Then, miRNA agomir or NC was injected stereotaxically into hippocampus of mice to explore the role of miRNA on GAS in response to LPS. Furthermore, Immunofluorescence and the hematoxylin and eosin (H&E) staining were employed to observe the cellular morphology. The protein levels of pro-inflammatory factors were evaluated by western blot. Finally, the target mRNA of miRNA was predicted using bioinformatics analysis. GO and KEGG enrichment analyses were conducted to clarify the potential function of target protein, which were visualized by bubble charts. Results: The behavioral data showed that mice in the LPS group had obvious depressive-anxiety-like behaviors, and 100 mg/kg GAS could improve these behavioral changes and alleviate the levels of pro-inflammatory cytokines in the hippocampus when mice were exposed to LPS for 6 h. Meanwhile, LPS-induced microglia and astrocyte activation in the CA1, CA2, CA3, and DG regions of the hippocampus were also reversed by GAS. Furthermore, miR-107-3p were screened out and verified for GAS in response to LPS. Importantly, miR-107-3p overexpression negatively abrogated the neuroprotective effects of GAS. Moreover, KPNA1 might be the target molecular of miR-107-3p. KPNA1 might regulate 12 neuroinflammation-related genes, which were mainly involved in cytokine-mediated signaling pathway. Conclusion: These results suggested that GAS might alleviate the LPS-induced neuroinflammation and depressive-anxiety-like behaviors in mice by downregulating miR-107-3p and upregulating the downstream target KPNA1. The indicates miR-107-3p may provide a new strategy for the treatment of CNS diseases.
| S-EPMC9773390 | biostudies-literature
Project description:To further elucidate the role of miRNAs, HTS was used to screen differential miRNAs. Mice hippocampus from the saline group, the LPS group, and the LPS+GAS group were removed to analyze using HTS.
2022-10-09 | GSE214909 | GEO
Project description:Neuroinflammation plays a role in the progression of several neurodegenerative disorders. We used a lipolysaccharide (LPS) model of neuroinflammation to characterize the gene expression changes underlying the inflammatory and behavioral effects of neuroinflammation. A single intracerebroventricular injection of LPS (5 ug) was administered into the lateral ventricle of mice and, 24 hours later, we examined gene expression in the cerebral cortex and hippocampus using microarray technology. Gene Ontology (GO) terms for inflammation and the ribosome were significantly enriched by LPS, whereas GO terms associated with learning and memory had decreased expression. We detected 224 changed transcripts in the cerebral cortex and 170 in the hippocampus. Expression of Egr1 (also known as Zif268) and Arc, two genes associated with learning and memory, was significantly lower in the cortex, but not hippocampus, of LPS-treated animals. Overall, altered expression of these genes may underlie some of the inflammatory and behavioral effects of neuroinflammation. Mice were given intracerebroventricular injections of saline vehicle (n = 4) or lipopolysaccharide (n = 4). Twenty-four hours later, we dissected the hippocampus and cerebral cortex and processed the tissue for microarray analysis. Gene expression changes observed in the microaray data were validated with quantitative real-time PCR.
2008-11-01 | E-GEOD-12284 | biostudies-arrayexpress
Project description:Hyperglycemia potentiates brain susceptibility to lipopolysaccharide-induced neuroinflammation by astrocytes reprogramming
| PRJNA1035940 | ENA
Project description:Gastrodia elata Blume (Orchidaceae) is an important Chinese medicine with several functional components. In the life cycle of G. elata, the orchid develops a symbiotic relationship with two compatible mycorrhizal fungi Mycena spp. and Armillaria mellea during seed germination to form vegetative propagation corm and vegetative growth to develop tubers, respectively. Gastrodin (p-hydroxymethylphenol-beta-D-glucoside) is the most important functional component in G. elata, and gastrodin significantly increases from vegetative propagation corms to tubers. To address the gene regulation mechanism in gastrodin biosynthesis in G. elata, a comparative analysis of de novo transcriptome sequencing among the vegetative propagation corms and tubers of G. elata and A. mellea was conducted using deep sequencing. Transcriptome comparison between the vegetative propagation corms and juvenile tubers of G. elata revealed 582 differentially expressed unigenes, of which 415 and 167 genes were, respectively up-regulated (fold-change â?¥ 2, p-value < 0.05) and down-regulated (fold-change â?¤ 0.5, p-value <0.05) in juvenile tubers. After Gene Ontology (GO) annotation and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analyses, forty-seven up-regulated unigenes with enzyme commission (EC) were assigned to 269 isogroups involved in 100 different pathways, and twenty-four down-regulated unigenes with enzyme commission (EC) were assigned to 586 isogroups, involved in 167 different pathways. The analysis of the isogroup genes from all pathways revealed that the two unigenes at locus 25,051 (one of monooxygenases) and locus 22,288 (one of glycosyltransferases) might participate in hydroxylation and glucosylation in the gastrodin biosynthetic pathway. The gene expression of the two unique unigenes encoding monooxygenase and glycosyltransferase significantly increases from vegetative propagation corms to tubers, and the molecular basis of gastrodin biosynthesis in the tubers of G. elata is proposed. Transcriptome comparative between vegetative propagation corms and tubers of G. elata, and between tubers of G. elata (symbiosis A. mellea) and A. mellea
2016-08-23 | E-GEOD-73633 | biostudies-arrayexpress
Project description:Gastrodia elata Blume (Orchidaceae) is an important Chinese medicine with several functional components. In the life cycle of G. elata, the orchid develops a symbiotic relationship with two compatible mycorrhizal fungi Mycena spp. and Armillaria mellea during seed germination to form vegetative propagation corm and vegetative growth to develop tubers, respectively. Gastrodin (p-hydroxymethylphenol-beta-D-glucoside) is the most important functional component in G. elata, and gastrodin significantly increases from vegetative propagation corms to tubers. To address the gene regulation mechanism in gastrodin biosynthesis in G. elata, a comparative analysis of de novo transcriptome sequencing among the vegetative propagation corms and tubers of G. elata and A. mellea was conducted using deep sequencing. Transcriptome comparison between the vegetative propagation corms and juvenile tubers of G. elata revealed 582 differentially expressed unigenes, of which 415 and 167 genes were, respectively up-regulated (fold-change ≥ 2, p-value < 0.05) and down-regulated (fold-change ≤ 0.5, p-value <0.05) in juvenile tubers. After Gene Ontology (GO) annotation and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analyses, forty-seven up-regulated unigenes with enzyme commission (EC) were assigned to 269 isogroups involved in 100 different pathways, and twenty-four down-regulated unigenes with enzyme commission (EC) were assigned to 586 isogroups, involved in 167 different pathways. The analysis of the isogroup genes from all pathways revealed that the two unigenes at locus 25,051 (one of monooxygenases) and locus 22,288 (one of glycosyltransferases) might participate in hydroxylation and glucosylation in the gastrodin biosynthetic pathway. The gene expression of the two unique unigenes encoding monooxygenase and glycosyltransferase significantly increases from vegetative propagation corms to tubers, and the molecular basis of gastrodin biosynthesis in the tubers of G. elata is proposed.
2016-08-23 | GSE73633 | GEO
Project description:Priestia aryabhattai 107 genome sequencing
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Project description:Escherichia phage 107 Genome sequencing
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Project description:Acidovorax sp. 107 transcriptome - Chisto_RNA_40
| PRJNA566718 | ENA
Project description:Hyperglycemia has been shown to modulate the immune response of peripheral immune cells and organs, but the impact of hyperglycemia on neuroinflammation within the brain remains elusive. In the present study, we provide evidences that streptozotocin (STZ)-induced hyperglycemic condition in mice drives a phenotypic switch of brain astrocytes to a proinflammatory and neurotoxic state, and increases brain vulnerability to mild peripheral inflammation. In particular, we found that hyperglycemia led to a significant increase in the astrocyte proliferation as determined by flow cytometric and immunohistochemical analyses of mouse brain. Transcriptomic analysis of isolated astrocytes from Aldh1l1CreER;tdTomato mice revealed that peripheral STZ injection induced astrocyte reprogramming into proliferative, proinflammatory and neurotoxic phenotype. Additionally, STZ-induced hyperglycemic condition significantly enhanced the infiltration of circulating myeloid cells into the brain and the disruption of blood-brain barrier in response to mild lipopolysaccharide (LPS) administration. Systemic hyperglycemia did not alter the intensity and sensitivity of peripheral inflammation in mice to LPS challenge, but increased the inflammatory potential of brain microglia. Furthermore, hyperglycemic mice exhibited a significant impairment in cognitive function after mild LPS administration compared to normoglycemic mice as determined by novel object recognition and Y-maze tasks. Taken together, these results demonstrate that hyperglycemia directly induces astrocyte reprogramming towards a proliferative and proinflammatory phenotype, which potentiates mild LPS-triggered inflammation within brain parenchymal regions.
2024-06-05 | GSE247033 | GEO