&lt;p&gt;Pharmacological Inhibition of Galectin-3 Ameliorates Diabetes-Associated Cognitive Impairment, Oxidative Stress and Neuroinflammation in vivo and in vitro&lt;/p&gt;

Yin, Qingqing; Chen, Jian; Ma, Shizhan; Dong, Chengliang; Zhang, Yue; Hou, Xunyao; Li, Shangbin; Liu, Bin

doi:10.2147/jir.s273858

Cited by 23 publications

(18 citation statements)

References 39 publications

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“…For example, Il1b can cause neurotoxicity ( 61 ), chemokines Ccl4 attracts infiltrating immune cells can exacerbate pathology. Lgals3 is the gene of galectin-3, our recent study showed that serum galectin-3 levels were remarkably increased not only in the of T2DM patients with mild cognitive impairment (MCI), but also in the serum and brain of T2DM mice, and we also confirmed galectin-3 was associated with neuroinflammation, oxidative stress, impaired learning and memory ( 53 , 62 ). Our results suggested that galectin-3 could be a promising therapeutic target candidate for treating DCD.…”

Section: Discussionsupporting

confidence: 70%

“…Trem2 has been used as a microglial activation marker and a general requirement for its activation ( 29 , 52 ). Galectin-3 can bind to the Trem2, activate microglia, and induce neuroinflammatory responses in an AD mouse model, our recent study confirmed that inhibition of endogenous Trem2 ligand ameliorates DCD by inhibiting oxidative stress and neuroinflammation ( 53 ). In addition, studies have shown that hyperglycemia leads to NF‐κB activation and triggering the release of proinflammatory cytokines ( 54 ).…”

Section: Discussionmentioning

confidence: 58%

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Single-Cell Sequencing Analysis of the db/db Mouse Hippocampus Reveals Cell-Type-Specific Insights Into the Pathobiology of Diabetes-Associated Cognitive Dysfunction

Liu

et al. 2022

Front. Endocrinol.

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Diabetes-associated cognitive decline (DCD), is one of the complications of diabetes, which is characterized by a series of neurophysiological and pathological abnormalities. However, the exact pathogenesis of DCD is still unknown. Single-cell RNA sequencing (scRNA-seq) could discover unusual subpopulations, explore functional heterogeneity and identify signaling pathways and potential markers. The aim of this research was to provide deeper opinion into molecular and cellular changes underlying DCD, identify different cellular types of the diabetic mice hippocampus at single-cell level, and elucidate the factors mediating the pathogenesis of DCD. To elucidate cell specific gene expression changes in the hippocampus of diabetic encephalopathy. Single-cell RNA sequencing of hippocampus from db/m and db/db mice was carried out. Subclustering analysis was performed to further describe microglial cell subpopulations. Interestingly using immunohistochemistry, these findings were confirmed at the protein level. Single cell analysis yielded transcriptome data for 14621 hippocampal cells and defined 11 different cell types. Analysis of differentially expressed genes in the microglia compartments indicated that infection- and immune system process- associated terms, oxidative stress and inflammation play vital roles in the progression of DCD. Compared with db/m mouse, experiments at the protein level supported the activation of microglia, increased expression of inflammatory factors and oxidative stress damage in the hippocampus of db/db mouse. In addition, a major finding of our research was the subpopulation of microglia that express genes related to pro-inflammatory disease-associated microglia (DAM). Our research reveals pathological alterations of inflammation and oxidative stress mediated hippocampal damage in the db/db mice, and may provide potential diagnostic biomarkers and therapeutic interventions for DCD.

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Section: Discussionsupporting

confidence: 70%

Section: Discussionmentioning

confidence: 58%

Single-Cell Sequencing Analysis of the db/db Mouse Hippocampus Reveals Cell-Type-Specific Insights Into the Pathobiology of Diabetes-Associated Cognitive Dysfunction

Liu

et al. 2022

Front. Endocrinol.

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“…In our recent study, MCP attenuated neuroinflammation, oxidative stress, and cognitive impairment in high-fat diet (HFD)/streptozotocin (STZ)-induced diabetic rats. In addition, MCP attenuated inflammation and oxidative stress in high glucose-stimulated BV-2 microglial cells [ 105 ]. Studies have shown that inhibiting Gal-3 can protect neurons from damage induced by inflammation, especially in the hippocampus and striatum [ 106 ].…”

Section: Main Textmentioning

confidence: 99%

“…In our previous study, we found that serum Gal-3 was significantly higher in T2DM patients with mild cognitive impairment (MCI) than in T2DM controls, even after adjustment for multiple potential confounders [ 110 ]. Similarly, Gal-3 levels in the serum and brain were increased in diabetic rats and were associated with neuroinflammation, oxidative stress, learning and memory impairment, while administration of MCP could reverse these outcomes [ 105 ]. Our findings indicated that Gal-3 might be a potential therapeutic target for cognitive impairment in diabetes.…”

Section: Main Textmentioning

confidence: 99%

Galectin-3: a key player in microglia-mediated neuroinflammation and Alzheimer's disease

Tan

Zheng

et al. 2021

Cell Biosci

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Alzheimer’s disease (AD) is the most common cause of dementia and is characterized by the deposition of extracellular aggregates of amyloid-β (Aβ), the formation of intraneuronal tau neurofibrillary tangles and microglial activation-mediated neuroinflammation. One of the key molecules involved in microglial activation is galectin-3 (Gal-3). In recent years, extensive studies have dissected the mechanisms by which Gal-3 modulates microglial activation, impacting Aβ deposition, in both animal models and human studies. In this review article, we focus on the emerging role of Gal-3 in biology and pathobiology, including its origin, its functions in regulating microglial activation and neuroinflammation, and its emergence as a biomarker in AD and other neurodegenerative diseases. These aspects are important to elucidate the involvement of Gal-3 in AD pathogenesis and may provide novel insights into the use of Gal-3 for AD diagnosis and therapy.

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“…Diabetes mellitus (DM) is a common chronic and progressive metabolic disease characterized by notably abnormal glucose metabolism [ 1 – 4 ]. It can cause huge economic burden to individuals and society.…”

Section: Introductionmentioning

confidence: 99%

Agomelatine might be more appropriate for elderly, depressed, type 2 diabetes mellitus patients than paroxetine/fluoxetine

Liang

Jia

Zhao

et al. 2021

Aging

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Agomelatine was a novel and melatonergic antidepressant. The present study was conducted to find out whether age was an important factor for agomelatine in treating depressed type 2 diabetes mellitus (T2DM) patients. In total, 193 depressed T2DM patients were included. There were 84 patients ranged from 27 years old to 49 years old (age phase I) ( n = 44 receiving agomelatine, n = 40 receiving paroxetine or fluoxetine), and 109 patients ranged from 50 years old to 70 years old (age phase II) ( n = 56 receiving agomelatine, n = 53 receiving paroxetine or fluoxetine). The Hamilton Depression Rating Scale (HDRS) score, Hamilton Anxiety Rating Scale (HARS) score, fasting plasma glucose (FPG), hemoglobin A1c (HbA1c) level and body mass index (BMI) were assessed after 12 weeks treatment. After treatment, we found that among patients in age phase I, there were no significant differences in final average HDRS score, HARS score, FPG, HbA1c level, BMI, response rate and remission rate between the two groups. However, among patients in age phase II, compared to patients receiving paroxetine or fluoxetine, patients receiving agomelatine had the significantly lower average HDRS score, HARS score, HbA1c level and BMI, and significantly higher response rate and remission rate. The incidence of treatment-related adverse events was similar between the two groups in both age phases. These results suggested that age was an important factor for agomelatine in treating depressed T2DM patients. Compared to paroxetine/fluoxetine, agomelatine might be more appropriate for elderly depressed T2DM patients.

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<p>Pharmacological Inhibition of Galectin-3 Ameliorates Diabetes-Associated Cognitive Impairment, Oxidative Stress and Neuroinflammation in vivo and in vitro</p>

Cited by 23 publications

References 39 publications

Single-Cell Sequencing Analysis of the db/db Mouse Hippocampus Reveals Cell-Type-Specific Insights Into the Pathobiology of Diabetes-Associated Cognitive Dysfunction

Single-Cell Sequencing Analysis of the db/db Mouse Hippocampus Reveals Cell-Type-Specific Insights Into the Pathobiology of Diabetes-Associated Cognitive Dysfunction

Galectin-3: a key player in microglia-mediated neuroinflammation and Alzheimer's disease

Agomelatine might be more appropriate for elderly, depressed, type 2 diabetes mellitus patients than paroxetine/fluoxetine

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