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ABSTRACT:
PROVIDER: PRJNA759189 | ENA |
REPOSITORIES: ENA
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Project description:Tanshinone IIA on Gut Microbiome in Diabetes-induced Cognitive Dysfunction
| PRJEB51712 | ENA
Project description:Cognitive dysfunction has been accepted as a possible complication of type 2 diabetes (T2D), but few studies revealed the potential roles of Long non‑coding RNAs (lncRNAs) in cognitive dysfunction in T2D. The purpose of the current research is to demonstrate the specific expression patterns of lncRNA-mRNA in the hippocampi of T2D db/db mice exhibiting cognitive impairment. In this study, the results from behavioral tests showed that T2D db/db mice displayed short-term and spatial working memory deficits compared to db/m mice. Furthermore, western blot analysis demonstrated that compared with db/m mice, p-GSK3β (ser9) protein levels were markedly elevated in T2D db/db mice (P<0.01). In addition, though not statistically significant, the ratio of p-Tau (Ser396) to Tau 46, α-Synuclein expression and p-GSK3α (ser21) expression were also relatively higher in T2D db/db mice than in db/m mice. The microarray profiling revealed that 75 lncRNAs and 26 mRNAs were obviously dysregulated in T2D db/db mice (>2.0 fold change, P<0.05). GO analysis demonstrated that the differentially expressed mRNAs participated in immune response, extracellular membrane-bounded organelle and extracellular region. KEGG analysis revealed that the differentially expressed mRNAs were mainly involved in one carbon pool by folate, glyoxylate and dicarboxylate metabolism, autophagy, glycine, serine and threonine metabolism and B cell receptor signaling pathway. An lncRNA‑mRNA coexpression network containing 71 lncRNAs and 26 mRNAs was built to investigate the interaction between lncRNA and mRNA. Collectively, these results revealed the differential hippocampal expression profiles of lncRNAs in T2D mice with cognitive dysfunction, and the findings from this study provide new clues for exploring the potential roles of lncRNAs in the pathogenesis of cognitive dysfunction in T2D.
2020-06-02 | GSE151294 | GEO
Project description:Background: The long-term high-fat, high-sugar diet exacerbates type 2 diabetes mellitus (T2DM)-related cognitive impairments. The negative impact of poor dietary patterns on brain development and neurological function may be related to gut microbiota disturbance. The role of phlorizin in mitigating glucose and lipid metabolism disorders is well documented. However, the protective effect of phlorizin on diabetes-related cognitive dysfunction is unclear. Therefore, the present study aimed to investigate the effect of dietary supplementation of phlorizin on high-fat and high-fructose diet (HFFD)-induced cognitive dysfunction and evaluate the crucial role of the microbiota-gut-brain axis. Results: Dietary supplementation of phlorizin for 14 weeks effectively prevented glucolipid metabolism disorder, spatial learning impairment, and memory impairment in HFFD mice. In addition, phlorizin improved the HFFD-induced decrease in synaptic plasticity, neuroinflammation, and excessive activation of microglia in the hippocampus. Transcriptomics analysis shows that the protective effect of phlorizin on cognitive impairment was associated with increased expression of neurotransmitters and synapse-related genes in the hippocampus. Phlorizin treatment alleviated colon microbiota disturbance, mainly manifested by an increase in gut microbiota diversity and the abundance of short-chain fatty acid (SCFA)-producing bacteria. The level of microbial metabolites, including SCFA, inosine 5'-monophosphate (IMP), and D (-)-beta-hydroxybutyric acid (BHB) were also significantly increased after phlorizin treatment. Moreover, integrating multiomics analysis observed tight connections between phlorizin-regulated genes, microbiota, and metabolites. Furthermore, removal of the gut microbiota via antibiotics treatment diminished the protective effect of phlorizin against HFFD-induced cognitive impairment, underscoring the critical role of the gut microbiota in mediating cognitive behavior. Importantly, supplementation with SCFA and BHB alone mimicked the regulatory effects of phlorizin on cognitive function. Conclusions: These results indicate that gut microbiota and their metabolites mediate the ameliorative effect of phlorizin on HFFD-induced cognitive impairment. Therefore, phlorizin can be used as an easy-to-implement nutritional therapy to prevent and alleviate metabolism-related neurodegenerative diseases by targeting the regulation of the microbiome-gut-brain axis.
2024-03-20 | GSE261887 | GEO
Project description:Radiotherapy is an important therapeutic option for the treatment of primary and metastatic brain tumors, and there is increasing concern about the side effects associated with it as survival time after treatment increases. By far, cognitive dysfunction is the most common radiation-induced central nervous system injury. Studies have shown that the hippocampus is involved in radiation-induced cognitive dysfunction. We constructed a model of radiation-induced cognitive dysfunction by irradiating the whole brain of one-month-old rats with 20 Gy, and analyzed the expression profiles in the hippocampus of rats with radiation-induced cognitive dysfunction using single-cell RNA sequencing (scRNA-seq).
2023-12-12 | GSE249426 | GEO
Project description:Type 2 diabetes is recognized as one of the primary contributors to cardiovascular diseases, with vascular endothelial dysfunction (VED) being a crucial mechanism underlying its development. In this study, we present the aberrant expressions of CircHMGCS1 and miR-4521 in diabetes-induced VED. Overexpression of CircHMGCS1 or silencing of miR-4521 expedited the onset of diabetes and aggravated VED. Mechanistically, CircHMGCS1 upregulated ARG1 by sequestering miR-4521, resulting in the inhibition of vascular NO secretion, enhanced adhesion molecules expression of VCAM1, ICAM1, ET-1, and increased ROS generation. Consequently, these events accelerated the impairment of vascular endothelial function. These findings underscore the physiological roles of CircRNA and miRNA in cardiovascular diseases triggered by diabetes and suggest that modulating the expression of CircHMGCS1 and miR-4521 could serve as a potential strategy for preventing endothelial cell dysfunction and the development of diabetes-associated cardiovascular diseases.
2024-08-08 | GSE237295 | GEO
Project description:Type 2 diabetes (T2D) is associated with increased risk of cognitive decline although the precise underlying pathogenesis remains obscure. Based on the single-cell RNA sequencing approach applied to the cerebral cortex of a T2D mouse model (db/db), we identified novel regulatory mechanisms underlying diabetes-associated cognitive deficits. Our data adds detail to the highly complex neurovascular pathology associated with T2D and highlights key cell-specific deficits in mitochondrial bioenergetics linked to neuroinflammation, which underlie T2D-linked cognitive impairment.
2023-06-26 | GSE217665 | GEO
Project description:Interventions: case series:None
Primary outcome(s): postoperative cognitive dysfunction;IL-6;IL-1;Gut flora
Study Design: Cohort study
| 79854 | ecrin-mdr-crc
Project description:To explore whether the cognitive effect of xanthohumol on mice is affected by the hypothalamic-pituitary-gonad system, and to fully reveal the potential regulatory mechanism of xanthohumol on mice cognition, we performed RNA-seq, miRNA-seq, and real-time qPCR to distinguish expression differences between xanthohumol and saline treated mice brain cells in both HPG dysfunction/normal conditions.This study provides comprehensive miRNA and mRNA expression profile data of xanthohumol and saline treated mice brain cells in HPG dysfunction and normal conditions, which advances our understanding of the regulation of cognitive impairment mediated by miRNA.
2023-05-01 | GSE174820 | GEO
Project description:High fat diet can lead to metabolic diseases such as obesity and diabetes known to be chronic inflammatory diseases with high prevalence worldwide. Recent studies have reported cognitive dysfunction in obese patients is caused by a high fat diet. Accordingly, such dysfunction is called “type 3 diabetes” or “diabetic dementia.” Although dysregulation of protein-coding genes has been extensively studied, profiling of non-coding RNAs including long non-coding RNAs (lncRNAs) and circular RNAs (circRNAs) has not been reported yet. Therefore, the objective of this study was to obtain profiles of diverse RNAs and determine their patterns of alteration in high fat fed brain cortex compared to normal brain cortex. To investigate regulatory roles of both coding and non-coding RNAs in high fat diet brain, we performed RNA sequencing of ribosomal RNA-depleted RNAs and identified genome-wide lncRNAs and circRNAs expression and co-expression patterns of mRNAs in high fat diet mouse brain cortex. Our results showed expression levels of mRNAs related to neurogenesis, synapse, and calcium signaling were highly changed in high fat diet fed cortex. In addition, numerous differentially expressed lncRNAs and circRNAs were identified. Our study provides valuable expression profiles and potential function of both coding and non-coding RNAs in high fat diet fed brain cortex.
2021-07-11 | GSE179711 | GEO