Amelioration of postoperative cognitive dysfunction in mice by mesenchymal stem cell-conditioned medium treatments is associated with reduced inflammation, oxidative stress and increased BDNF expression in brain tissues

Jiang, Ye; Gao, Hong; Yuan, Hongbin; Xu, Haitao; Tian, Mou-Li; Du, Guizhi; Xie, Wenpin

doi:10.1016/j.neulet.2019.134372

Cited by 17 publications

(19 citation statements)

References 14 publications

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“…Mesenchymal stem cell-conditioned medium (MSC-CM) ameliorates POCD in mice. The therapeutic effects of MSC-CM in a mouse model of POCD were associated with a reduction in inflammation, attenuation of oxidative stress, and an increased in BDNF expression in brain tissues ( Jiang et al, 2019 ). Edaravone, a powerful free radical scavenger, can attenuate POCD in aged mice.…”

Section: Advances In Treatmentmentioning

confidence: 99%

Update on the Mechanism and Treatment of Sevoflurane-Induced Postoperative Cognitive Dysfunction

Wang

Chen

Zhang

et al. 2021

Front. Aging Neurosci.

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Sevoflurane is one of the most widely used anesthetics for the induction and maintenance of general anesthesia in surgical patients. Sevoflurane treatment may increase the incidence of postoperative cognitive dysfunction (POCD), and patients with POCD exhibit lower cognitive abilities than before the operation. POCD affects the lives of patients and places an additional burden on patients and their families. Understanding the mechanism of sevoflurane-induced POCD may improve prevention and treatment of POCD. In this paper, we review the diagnosis of POCD, introduce animal models of POCD in clinical research, analyze the possible mechanisms of sevoflurane-induced POCD, and summarize advances in treatment for this condition.

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Section: Advances In Treatmentmentioning

confidence: 99%

Update on the Mechanism and Treatment of Sevoflurane-Induced Postoperative Cognitive Dysfunction

Wang

Chen

Zhang

et al. 2021

Front. Aging Neurosci.

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“…In addition to its effects on NSCs, GM-CSF has been shown to mobilize mesenchymal stem cells (MSCs) from the bone marrow and to enhance their differentiation and migration in response to injury (109,110). MSCs have been reported to have beneficial cognitive and regenerative effects and are being investigated as potential positive effectors in several neurological disorders, including AD, PD, and spinal cord injury (111)(112)(113)(114)(115)(116)(117).…”

Section: Discussionmentioning

confidence: 99%

Pro-inflammatory Cytokine GM-CSF Improves Learning/Memory and Brain Pathology in Dp16 Down Syndrome Mice and Improves Learning/Memory in Wild-Type Mice

Ahmed

Wang

Elos

et al. 2021

Preprint

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Down syndrome (DS) is characterized by chronic neuroinflammation, peripheral inflammation, astrogliosis, imbalanced excitatory/inhibitory neuronal function, and cognitive deficits in both humans and mouse models. Suppression of inflammation has been proposed as a therapeutic approach to treating DS co-morbidities, including intellectual disability (DS/ID). Conversely, we discovered previously that treatment with the pro-inflammatory cytokine granulocyte-macrophage colony-stimulating factor (GM-CSF) improved cognition and reduced biomarkers of brain pathology in humans with Alzheimer·s disease (AD), another inflammatory disorder, and in a mouse model of AD. To investigate the effects of GM-CSF treatment on DS/ID, we assessed behavior and brain pathology in 12-14 month-old DS mice (Dp[16]1Yey) and their wild-type (WT) littermates, neither of which develop amyloid, and found that GM-CSF treatment improved performance in the radial arm water maze in both Dp16 and WT mice compared to placebo. Dp16 mice also showed abnormal astrocyte morphology and aggregation and fewer calretinin-positive interneurons, both of which were improved by GM-CSF treatment. These findings suggest that stimulating and/or modulating inflammation and the innate immune system with GM-CSF treatment may enhance cognition in both people with DS/ID and in the typical aging population.

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“… 23 , 36 Neurotrophic factors such as BDNF and NGF are also enhanced. 70 , 71 All these mediators have indirect effects on the inhibition of neuroinflammation; (iii) microglial M1/M2 polarization. In the classic M1 state, the expression of CD86 and the release of pro-inflammatory cytokines are increased, including TNF-α, iNOS, IL-1β, IL-6, IL-12, and IL-23.…”

Section: Transplanted Bmmscs Inhibit Neuroinflammationmentioning

confidence: 99%

Functional Mechanism of Bone Marrow-Derived Mesenchymal Stem Cells in the Treatment of Animal Models with Alzheimer’s Disease: Inhibition of Neuroinflammation

Qin¹,

Li²,

Wang³

2021

JIR

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The transplantation of bone marrow-derived mesenchymal stem cells (BMMSCs) alleviates neuropathology and improves cognitive deficits in animal models with Alzheimer’s disease. However, the underlying mechanisms remain to be determined. Available data demonstrate transplanted BMMSCs can inhibit neuroinflammation, which may be related to microglial M1/M2 polarization and is regulated by the secretion of autocrine and paracrine cytokines. BMMSCs also mitigate Aβ plaques and Tau tangles in the brain, which may be associated with the recruitment of peripheral blood monocytes and the subsequent comprehensive effects. The therapeutic effects of stem cells involve potential mechanisms such as immunomodulation, apoptosis, and proliferation. BMMSC-mediated functional reconstruction through dynamic remodeling develops a novel balance. Herein, present review recapitulates the molecular basis of BMMSC-assisted biological processes and summarizes the possible mechanisms related to the interaction between BMMSCs and microglia. The transplanted BMMSCs can suppress neuroinflammation that plays a key role in the pathogenesis of Alzheimer’s disease.

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Amelioration of postoperative cognitive dysfunction in mice by mesenchymal stem cell-conditioned medium treatments is associated with reduced inflammation, oxidative stress and increased BDNF expression in brain tissues

Cited by 17 publications

References 14 publications

Update on the Mechanism and Treatment of Sevoflurane-Induced Postoperative Cognitive Dysfunction

Update on the Mechanism and Treatment of Sevoflurane-Induced Postoperative Cognitive Dysfunction

Pro-inflammatory Cytokine GM-CSF Improves Learning/Memory and Brain Pathology in Dp16 Down Syndrome Mice and Improves Learning/Memory in Wild-Type Mice

Functional Mechanism of Bone Marrow-Derived Mesenchymal Stem Cells in the Treatment of Animal Models with Alzheimer’s Disease: Inhibition of Neuroinflammation

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