Administration of rTMS Alleviates Stroke-Induced Cognitive Deficits by Modulating miR-409-3p/CTRP3/AMPK/Sirt1 Axis

Wu, Tianya; Tang, Chunrong; Fan, Junwei; Tao, Jian

doi:10.1007/s12031-021-01924-5

Cited by 9 publications

(9 citation statements)

References 30 publications

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“…These results indicate that magnoflorine has a neuroprotective effect through the regulation of oxidative stress and autophagy activation in a rat MCAO model. AMPK, as a cellular energy detector, has been proven to play a crucial role in the prevention of neuron injuries because of its activation influence for Sirt1 [ 17 , 35 ]. Studies have shown that the activation of the AMPK/Sirt1 pathway protects against MCAO-induced impairments, which benefits cognitive function and neuron viability [ 35 ].…”

Section: Discussionmentioning

confidence: 99%

“…AMPK, as a cellular energy detector, has been proven to play a crucial role in the prevention of neuron injuries because of its activation influence for Sirt1 [ 17 , 35 ]. Studies have shown that the activation of the AMPK/Sirt1 pathway protects against MCAO-induced impairments, which benefits cognitive function and neuron viability [ 35 ]. Our data showed that magnoflorine administration contributed to the activation of the Sirt1/AMPK pathway under cerebral ischemic conditions.…”

Section: Discussionmentioning

confidence: 99%

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Magnoflorine Attenuates Cerebral Ischemia-Induced Neuronal Injury via Autophagy/Sirt1/AMPK Signaling Pathway

Hai

Chang

Xia

et al. 2022

Evidence-Based Complementary and Alternative Medicine

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Ischemic stroke is a common cause of permanent disability worldwide. Magnoflorine has been discovered to have good antioxidation, immune regulation, and cardiovascular system protection functions. However, whether magnoflorine treatment protects against cerebral ischemic stroke and the mechanism of such protection remains unknown. Here, we investigated the effect of magnoflorine on the development of ischemic stroke disorder in rats. A middle cerebral artery occlusion (MCAO) model followed by 24 h reperfusion after 90 min ischemia was used. The rats were treated with magnoflorine (10 mg/kg or 20 mg/kg) for 15 consecutive days. The neurological deficit scores, cerebral infarct volume, and brain water content were measured. The neuronal density was determined using Nissl and NeuN staining. The oxidative stress levels were determined using commercial kits. Immunofluorescence staining of LC3 and western blot assay for LC3 and p62 were used to assess autophagy. Magnoflorine treatment significantly reduced the cerebral infarct volume and brain water content and improved the neurological deficit scores in the rat MCAO model. In addition, magnoflorine ameliorated neuronal injury and neuron density in the cortex of rats. Magnoflorine also prevented oxidative damage following ischemia, reflected by the decrement of nitric oxide and malondialdehyde and the increase of glutathione (GSH) and GSH peroxidase. Moreover, the fluorescence intensity of LC3 and the ratio of LC3-II to LC3-I were remarkably downregulated in ischemic rat administration of magnoflorine. Finally, the expression levels of p62, sirtuin 1 (Sirt1), and phosphorylated-adenosine monophosphate-activated protein kinase (AMPK) were upregulated with magnoflorine. Magnoflorine attenuated the cerebral ischemia-induced neuronal damage, which was possibly associated with antioxidative stress, suppression of autophagy, and activation of the Sirt1/AMPK pathway in the rats.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Magnoflorine Attenuates Cerebral Ischemia-Induced Neuronal Injury via Autophagy/Sirt1/AMPK Signaling Pathway

Hai

Chang

Xia

et al. 2022

Evidence-Based Complementary and Alternative Medicine

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“…By comparison with the CN group, MMSE score (28 (27-29) vs. 13 (9)(10)(11)(12)(13)(14)(15)(16)(17)(18)(19), p < 0.0001) and MoCA score (28 (26-29) vs. 8 (4-13), p < 0.0001) were reduced in the AD group, while ADL score (16 (16-16) vs. 35 , p < 0.0001) and CDR-SB score (0 (0-0) vs. 12 (7-16), p < 0.0001) were increased (Table 1 1 and Figure S2). Correlations between any two of the three CTRPs members were statistically significant among all subjects (Figure S3).…”

Section: Comparison Of Baseline Data Between Two Groupsmentioning

confidence: 99%

“…10 Repetitive transcranial magnetic stimulation alleviated learning and memory impairment in rats receiving middle cerebral artery occlusion (MCAO) by activating the CTRP3-signaling pathway. 11 In addition to the adipose tissue, CTRP4 is synthesized and secreted by neurons at an early stage of brain development and forms a variety of oligomeric complexes widely distributed in brains of humans, mice, and zebrafish. [12][13][14][15] Lacking of CTRP4 impaired hippocampaldependent associative learning and memory abilities in mice in the fear-conditioning paradigm by altering expressions of cognitionrelated genes in hippocampus and cortex.…”

Section: Mounting Evidence Has Proved Complicated Associations Ofmentioning

confidence: 99%

“…The overexpression of CTRP3 attenuated neuronal apoptosis and neuroinflammation, and improved learning and memory abilities in elderly rats anesthetized with sevoflurane 10 . Repetitive transcranial magnetic stimulation alleviated learning and memory impairment in rats receiving middle cerebral artery occlusion (MCAO) by activating the CTRP3‐signaling pathway 11 . In addition to the adipose tissue, CTRP4 is synthesized and secreted by neurons at an early stage of brain development and forms a variety of oligomeric complexes widely distributed in brains of humans, mice, and zebrafish 12–15 .…”

Section: Introductionmentioning

confidence: 99%

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Association between plasma CTRPs with cognitive impairment and neurodegeneration of Alzheimer's disease

Huang,

Zhao,

Wang

et al. 2024

CNS Neurosci Ther

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AimsRecent evidence indicated the biological basis of complement 1q (C1q)/tumor necrosis factor (TNF)‐related protein (CTRP) 3, 4, and 14 for affecting brain structure and cognitive function. Thus, we aimed to investigate the association between plasma CTRPs with Alzheimer's disease (AD).MethodsA multicenter, cross‐sectional study recruited patients with AD (n = 137) and cognitively normal (CN) controls (n = 140). After the data collection of demographic characteristics, lifestyle risk factors, and medical history, plasma levels of tau phosphorylated at threonine 217 (pT217), pT181, neurofilament light (NfL), CTRP3, 4, and 14 were examined and compared. Multivariate logistic regression analysis was applied to determine associations of plasma CTPRs with the presence of AD. The correlation analysis was used to explore correlations between plasma CTPRs with scores of Mini‐Mental State Examination (MMSE), Montreal Cognitive Assessment (MoCA), Activities of Daily Living (ADL) scale, and Clinical Dementia Rating Sum of Boxes (CDR‐SB), and levels of plasma pT217, pT181, and NfL. Receiver‐operating characteristic (ROC) analysis and Delong's test were used to determine the diagnostic power of plasma CTPRs.ResultsPlasma levels of CTRP3, 4, and 14 were higher in AD group than those in CN group. After adjusting for conventional risk factors, CTRP3, CTRP4, and CTRP14 were associated with the presence of AD. In AD patients, CTRP3 was negatively correlated with scores of MMSE and MoCA, while positively correlated with ADL score, CDR‐SB score, pT217, and pT181; CTRP4 was positively correlated with CDR‐SB score, pT181, and NfL; CTRP14 was negatively correlated with MMSE score, while positively correlated with CDR‐SB score, pT217, and NfL. An independent addition of CTRP3 and 4 to the basic model combining age, sex, years of education, APOE4 status, BMI, TG, and HDL‐C led to a significant improvement in diagnostic power for AD, respectively.ConclusionsAll the findings preliminarily uncovered associations between plasma CTRPs and AD and suggested the potential of CTRPs as a blood‐derived biomarker for AD.

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Long-term iTBS Improves Neural Functional Recovery by Reducing the Inflammatory Response and Inhibiting Neuronal Apoptosis Via miR-34c-5p/p53/Bax Signaling Pathway in Cerebral Ischemic Rats

Wang

Yang

et al. 2023

Neuroscience

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Administration of rTMS Alleviates Stroke-Induced Cognitive Deficits by Modulating miR-409-3p/CTRP3/AMPK/Sirt1 Axis

Cited by 9 publications

References 30 publications

Magnoflorine Attenuates Cerebral Ischemia-Induced Neuronal Injury via Autophagy/Sirt1/AMPK Signaling Pathway

Magnoflorine Attenuates Cerebral Ischemia-Induced Neuronal Injury via Autophagy/Sirt1/AMPK Signaling Pathway

Association between plasma CTRPs with cognitive impairment and neurodegeneration of Alzheimer's disease

Long-term iTBS Improves Neural Functional Recovery by Reducing the Inflammatory Response and Inhibiting Neuronal Apoptosis Via miR-34c-5p/p53/Bax Signaling Pathway in Cerebral Ischemic Rats

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