Exercise ameliorates post-stroke depression by inhibiting PTEN elevation-mediated upregulation of TLR4/NF-κB/NLRP3 signaling in mice

Li, Congqin; Xu, Xiangyu; Wang, Ziwei; Wang, Yuyang; Cheng, Jing; Chen, Songfeng; Liu, Heng-Jian; Wan, Qi; Wang, Qiang

doi:10.1016/j.brainres.2020.146777

Cited by 28 publications

(21 citation statements)

References 54 publications

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“…Babri et al observed that acute administration of loganin could improve spatial memory in diabetic rats [ 40 ]. Wang et al verified that loganin alleviates intestinal epithelial inflammation by regulating the TLR4/NF-κB and JAK/STAT3 signaling pathways [ 41 ]. Chao et al exhibited that loganin has beneficial effects on Schwann cells by blocking Smad2 signaling induced by TNF-α [ 42 ].…”

Section: Discussionmentioning

confidence: 99%

Loganin Attenuates High Glucose-Induced Schwann Cells Pyroptosis by Inhibiting ROS Generation and NLRP3 Inflammasome Activation

Cheng

Chu²,

Chen

et al. 2020

Cells

109

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Diabetic peripheral neuropathy (DPN) is caused by hyperglycemia, which induces oxidative stress and inflammatory responses that damage nerve tissue. Excessive generation of reactive oxygen species (ROS) and NOD-like receptor protein 3 (NLRP3) inflammasome activation trigger the inflammation and pyroptosis in diabetes. Schwann cell dysfunction further promotes DPN progression. Loganin has been shown to have antioxidant and anti-inflammatory neuroprotective activities. This study evaluated the neuroprotective effect of loganin on high-glucose (25 mM)-induced rat Schwann cell line RSC96 injury, a recognized in vitro cell model of DPN. RSC96 cells were pretreated with loganin (0.1, 1, 10, 25, 50 μM) before exposure to high glucose. Loganin’s effects were examined by CCK-8 assay, ROS assay, cell death assay, immunofluorescence staining, quantitative RT–PCR and western blot. High-glucose-treated RSC96 cells sustained cell viability loss, ROS generation, NF-κB nuclear translocation, P2 × 7 purinergic receptor and TXNIP (thioredoxin-interacting protein) expression, NLRP3 inflammasome (NLRP3, ASC, caspase-1) activation, IL-1β and IL-18 maturation and gasdermin D cleavage. Those effects were reduced by loganin pretreatment. In conclusion, we found that loganin’s antioxidant effects prevent RSC96 Schwann cell pyroptosis by inhibiting ROS generation and suppressing NLRP3 inflammasome activation.

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Section: Discussionmentioning

confidence: 99%

Loganin Attenuates High Glucose-Induced Schwann Cells Pyroptosis by Inhibiting ROS Generation and NLRP3 Inflammasome Activation

Cheng

Chu²,

Chen

et al. 2020

Cells

109

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“…In addition, both aerobic regimens reduced pro-BDNF levels in CA3 and DG regions, which preferentially binds with p75 NTR , triggering proapoptotic and synaptic withdrawal [37,132]. Using the same protocol based on SLT, HIIT could decrease neuronal death in the DG by reducing the expression of the TLR4/NF-kB/NLRP3 pathway and the depression [133]. Earlier poststroke HIIT also downregulates pro-and anti-inflammatory Both HIIT ➚ FNDC5 and Cyt C in the contralesional cortex ➚ indicate an increase; ➘ indicate a decrease; BDNF: brain-derived neurotrophic factor; proBDNF: precursor brain-derived neurotrophic factor; mBDNF: mature brain-derived neurotrophic factor; VEGF: vascular endothelial growth factor; IGF-1: insulin-like growth factor 1; NKCC1: Na + -K + -2Cl − cotransporter; KCC2: K + -Cl − cotransporter; HRR: heart rate reserve; HI: high-intensity; LI; low-intensity; HIIT: high-intensity interval training; MICT: moderate-intensity continue training; HHb: deoxyhemoglobin; THb: total hemoglobin; SLT: speed at lactate threshold; Smax: maximal speed; tMCAO: transient middle cerebral artery occlusion; DG: dentate gyrus; TrkB: Tropomyosin receptor kinase B; p75 NTR : p75 neurotrophin receptor; NR2A: N-methyl-D-aspartate subtype glutamate receptor leading to LTP; NR2B: N-methyl-D-aspartate subtype glutamate receptor producing LTD, pTrkB: phosphorylated form of tropomyosin receptor kinase B; FNDC5: fibronectin type III domain-containing protein 5; Cyt C: Cytochrome C. ➚ indicate an increase; ⟺ indicate a maintenance; BDNF: brain-derived neurotrophic factor; VEGF: vascular endothelial growth factor; IGF-1: insulin-like growth factor 1; HRR: heart rate reserve; HI: high-intensity; LI; low-intensity; HIIT: high-intensity interval training; MICT: moderate-intensity.…”

Section: In Rodents With Cerebral Ischemiamentioning

confidence: 99%

Section: In Rodentsmentioning

confidence: 99%

Is High-Intensity Interval Training Suitable to Promote Neuroplasticity and Cognitive Functions after Stroke?

Hugues

Pellegrino

Rivera

et al. 2021

IJMS

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Stroke-induced cognitive impairments affect the long-term quality of life. High-intensity interval training (HIIT) is now considered a promising strategy to enhance cognitive functions. This review is designed to examine the role of HIIT in promoting neuroplasticity processes and/or cognitive functions after stroke. The various methodological limitations related to the clinical relevance of studies on the exercise recommendations in individuals with stroke are first discussed. Then, the relevance of HIIT in improving neurotrophic factors expression, neurogenesis and synaptic plasticity is debated in both stroke and healthy individuals (humans and rodents). Moreover, HIIT may have a preventive role on stroke severity, as found in rodents. The potential role of HIIT in stroke rehabilitation is reinforced by findings showing its powerful neurogenic effect that might potentiate cognitive benefits induced by cognitive tasks. In addition, the clinical role of neuroplasticity observed in each hemisphere needs to be clarified by coupling more frequently to cellular/molecular measurements and behavioral testing.

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“…Pathway analysis suggested that Epicedium may play an antidepressant role by regulating TNF signaling pathway, dopaminergic synapse, and prolactin signaling pathway. TNF, dopamine, calcium signaling pathway, prolactin, and I-kappaB kinase/NF-kappaB signaling play important roles in the pathogenesis of depression [50][51][52]. As a messenger, Ca 2+ is involved in the regulation of various neural cell functions, such as the release of neurotransmitters, the construction of cells, and the activation of enzyme system.…”

Section: Discussionmentioning

confidence: 99%

Molecular mechanism of Epicedium treatment for depression based on network pharmacology and molecular docking technology

Dong

Tao

Xue

et al. 2021

BMC Complement Med Ther

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Background Increasing attention has been paid to the effect of Epimedium on the nervous system, particularly anti-depression function. In the present study, we applied network pharmacology to introduce a testable hypothesis on the multi-target mechanisms of Epicedium against depression. Methods By reconstructing the network of protein–protein interaction and drug–component–target, we predicted the key protein targets of Epicedium for the treatment of depression. Then, through molecular docking, the interaction of the main active components of Epicedium and predicted candidate targets were verified. Results Nineteen active compounds were selected from Epicedium. There were 200 targets associated with Epicedium and 537 targets related to depression. The key targets of Epicedium for treating depression were IL6, VEGFA, AKT1, and EGF. According to gene ontology functional enrichment analysis, 22 items of biological process (BP), 13 items of cell composition (CC) and 9 items of molecular function (MF) were obtained. A total of 56 signaling pathways (P < 0.05) were identified by Kyoto Encyclopedia of Genes and Genomes analysis, mainly involving depression-related pathways such as dopaminergic synapse, TNF signaling pathway, and prolactin signaling pathway. The results of molecular docking showed that the most important activity components, including luteoklin, quercetin and kaempferol, were well combined with the key targets. Conclusions Luteoklin, quercetin, kaempferol and other active compounds in Epicedium can regulate multiple signaling pathways and targets such as IL6, AKT1, and EGF, therefore playing therapeutic roles in depression.

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Exercise ameliorates post-stroke depression by inhibiting PTEN elevation-mediated upregulation of TLR4/NF-κB/NLRP3 signaling in mice

Cited by 28 publications

References 54 publications

Loganin Attenuates High Glucose-Induced Schwann Cells Pyroptosis by Inhibiting ROS Generation and NLRP3 Inflammasome Activation

Loganin Attenuates High Glucose-Induced Schwann Cells Pyroptosis by Inhibiting ROS Generation and NLRP3 Inflammasome Activation

Is High-Intensity Interval Training Suitable to Promote Neuroplasticity and Cognitive Functions after Stroke?

Molecular mechanism of Epicedium treatment for depression based on network pharmacology and molecular docking technology

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