Cranial electrotherapy stimulation alleviates depression-like behavior of post-stroke depression rats by upregulating GPX4-mediated BDNF expression

Wang, Xiaoju; Xia, Peng; Song, Jiulong; Yang, Tao; Yu, Changjun; Cheng, Kai; Chen, Anliang; Li, Xueping

doi:10.1016/j.bbr.2022.114117

Cited by 6 publications

(4 citation statements)

References 41 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Accumulating evidence shows that dysregulation of synaptic plasticity increases vulnerability to depression, especially the loss of neurotrophic factors (Aleksandrova et al, 2019; Monteiro et al, 2017). BDNF, a key determinant of neuroplasticity highly expressed in the hippocampus (Wang, Xia, et al, 2022), serves as an essential mediator linking neuroplastic changes and antidepressants (Bjorkholm & Monteggia, 2016). TrkB is a functional receptor for BDNF, and it is widely distributed on presynaptic and postsynaptic membranes of dendritic spines, axons and neuronal cell bodies (Bjorkholm & Monteggia, 2016).…”

Section: Discussionmentioning

confidence: 99%

Kaempferol‐3‐O‐sophoroside (PCS‐1) contributes to modulation of depressive‐like behaviour in C57BL/6J mice by activating AMPK

Wang,

Hu,

Liu

et al. 2023

British J Pharmacology

View full text Add to dashboard Cite

Background and PurposeKaempferol‐3‐O‐sophoroside (PCS‐1) is the main component in Crocus sativus (Saffron), a traditional herb with mood‐enhancing properties. Adenosine monophosphate‐activated protein kinase (AMPK) is a potential therapeutic target for depression. This study aims to explore the antidepressive‐like properties of PCS‐1 and its AMPK activation to confirm AMPK as a target for antidepression.Experimental ApproachCorticosterone (CORT)‐induced PC12 cell injury served as an in‐vitro model to evaluate the neuroprotective effect of PCS‐1. Neuro‐2a cells and primary neurons were utilized to evaluate the synaptogenesis role of PCS‐1. CORT‐induced mouse depression model and chronic unpredictable mild stress (CUMS) model were used to assess the antidepressive‐like properties of PCS‐1 through behavioral tests, magnetic resonance imaging, and biochemical index measurements. Western blot and immunofluorescence assays were used to study the mechanisms of PCS‐1. Cellular thermal shift assay was used to confirm the binding target.Key ResultsPCS‐1 (12.5–50 μM) ameliorated CORT‐induced PC12 cell damage, oxidative stress and inflammation. PCS‐1 (12.5–50 μM) alone promoted an increase in synapses in Neuro‐2a cells and primary neurons. Oral administration of PCS‐1 (10 and 20 mg/kg) ameliorated weight loss, dyskinesia, and hippocampal volume reduction induced by CORT and CUMS. Mechanistically, PCS‐1 bound to AMPK to improve the expression of brain‐derived neurotrophic factor (BDNF) and induce autophagy.Conclusion and ImplicationsPCS‐1 binds to AMPK to promote BDNF production and autophagy enhancement, ultimately achieving antidepressant effects. This study provides support for the clinical application of saffron petals and provides further evidence for AMPK as a potential target for antidepression.

show abstract

Section: Discussionmentioning

confidence: 99%

Kaempferol‐3‐O‐sophoroside (PCS‐1) contributes to modulation of depressive‐like behaviour in C57BL/6J mice by activating AMPK

Wang,

Hu,

Liu

et al. 2023

British J Pharmacology

View full text Add to dashboard Cite

show abstract

“… 34 RSL3 has been widely reported to be an inducer of ferroptosis. 35 Aim to assess the effect of miR-342-5p on ferroptosis under ischemic and secondary reperfusion conditions, the mice were randomly divided into 4 groups, consisting of the Sham group, MCAO/R group, MCAO/R + RSL3 + NC mimic group, and MCAO/R + RSL3 + miR-342-5p mimic group. RSL3 (S8155, Selleck, Houston, TX, USA), dissolved in the solvent dimethylsulfoxide (DMSO), was intraperitoneally injected into the mice in the later 2 groups at a dose of 30 mg/kg within 24 h before the MCAO/R operation.…”

Section: Methodsmentioning

confidence: 99%

Circ_0008146 Exacerbates Ferroptosis via Regulating the miR-342-5p/ACSL4 Axis After Cerebral Ischemic/Reperfusion

Liu,

Peng,

Wang

et al. 2024

JIR

View full text Add to dashboard Cite

Purpose Acute ischemic stroke (AIS) has seriously threatened people’s health worldwide and there is an urge need for early diagnosis and effective treatment of AIS. This research intended to clarify the regulatory role of circ_0008146/miR-342-5p/ACSL4 axis in AIS. Methods High-throughput small RNA sequencing analysis was adapted to identify differentially expressed miRNAs between the AIS and control group. The circ_0008146, miR-342-5p, and ACSL4 levels were detected by qRT-PCR. Middle cerebral artery occlusion/reperfusion (MCAO/R) models were constructed in C57BL/6J mice. Assay kits were used to determine Fe 2+ levels and a battery of oxidative stress and lipid peroxidation indicators, including ROS, MDA, LPO, SOD and GSH/GSSG ratio. The protein levels of ACSL4 were measured by Western blot. The behavioral function was assessed using neurobehavioral tests. TTC staining was employed to visualize infarction size. Nissl staining was adapted to detect histopathological changes. Receiver operating characteristic curve and correlation analysis were applied to investigate the clinical value and association of miR-342-5p and ACSL4. Results A total of 44 AIS patients and 49 healthy controls were enrolled in our study. The small RNA sequencing unveiled a significant decrease in miR-342-5p levels in AIS patients. MiR-342-5p inhibited oxidative stress and RSL3-induced ferroptosis after cerebral ischemic/reperfusion injury in vivo by targeting ferroptosis-related gene ACSL4. Circ_0008146 acted as a sponge of miR-342-5p, and overexpression of circ_0008146 increased neurological deficits and brain injury in mice. Circ_0008146 contributed to ferroptosis in cerebral infarction via sponging miR-342-5p to regulate ACSL4. Plasma miR-342-5p and ACSL4 demonstrated significant correlation and good diagnostic value for AIS patients. Conclusion This study provides the first in vivo evidence to show that circ_0008146 exacerbates neuronal ferroptosis after AIS via the miR-342-5p/ACSL4 axis. Furthermore, miR-342-5p/ACSL4 axis holds promise as a viable therapeutic target and practical biomarkers for AIS patients.

show abstract

“…It not only regulates synaptic plasticity and neuronal development but is also an important factor in the regulation of mood disorders . Berton et al found in various animal models of depression that BDNF levels in the nucleus accumbens of depression model rats remained unchanged or even increased (Berton et al 2006;Dandekar et al 2019), whereas BDNF levels in the hippocampus decreased (Rahmani et al 2020;Wang et al 2023). Pro-BDNF is a BDNF precursor that is cleaved into mature BDNF .…”

Section: Neurotrophic Factors Regulate Synaptic Plasticitymentioning

confidence: 99%

A New Perspective on Hippocampal Synaptic Plasticity and Post-stroke Depression

Sun

Cui

Min

et al. 2023

Preprint

View full text Add to dashboard Cite

Post-stroke depression (PSD), a common complication after stroke, severely affects the recovery and quality of life of patients with stroke. Owing to its complex mechanisms, PSD treatment remains highly challenging. Hippocampal synaptic plasticity is one of the key factors leading to PSD; however, the precise molecular mechanisms remain unclear. Numerous studies have found that neurotrophic factors, protein kinases, and neurotransmitters influence depressive behavior by modulating hippocampal synaptic plasticity. This review further elaborates on the role of hippocampal synaptic plasticity in PSD by summarizing recent research and analyzing possible molecular mechanisms. Evidence for the correlation between hippocampal mechanisms and PSD helps to better understand the pathological process of PSD and improve its treatment.

show abstract

Cranial electrotherapy stimulation alleviates depression-like behavior of post-stroke depression rats by upregulating GPX4-mediated BDNF expression

Cited by 6 publications

References 41 publications

Kaempferol‐3‐O‐sophoroside (PCS‐1) contributes to modulation of depressive‐like behaviour in C57BL/6J mice by activating AMPK

Kaempferol‐3‐O‐sophoroside (PCS‐1) contributes to modulation of depressive‐like behaviour in C57BL/6J mice by activating AMPK

Circ_0008146 Exacerbates Ferroptosis via Regulating the miR-342-5p/ACSL4 Axis After Cerebral Ischemic/Reperfusion

A New Perspective on Hippocampal Synaptic Plasticity and Post-stroke Depression

Contact Info

Product

Resources

About