Cordycepin Ameliorates Spaceflight-Induced Osteoporosis by Preventing BMSCs Oxidative Stress and Senescence via Interacting with PI3K p110α and Regulating PI3K/Akt/FOXO3 Signalling DOI Creative Commons

Yu Zhai,

Yuyao Zhang, Kexin Xu

et al.

Free Radical Biology and Medicine, Journal Year: 2024, Volume and Issue: unknown

Published: Dec. 1, 2024

Language: Английский

The monoterpenoids of Paeoniae radix rubra alleviate dopaminergic neuronal injury of Parkinson's disease by inhibiting Bach1 and activating Nrf2/ARE pathway DOI
Xuwen Liu, Xinyuan Li, Mengmeng Li

et al.

Food Bioscience, Journal Year: 2025, Volume and Issue: 63, P. 105808 - 105808

Published: Jan. 1, 2025

Language: Английский

Citations

2

Costunolide normalizes neuroinflammation and improves neurogenesis deficits in a mouse model of depression through inhibiting microglial Akt/mTOR/NF-κB pathway DOI Creative Commons

S. Zhang,

Qiao Deng,

Cheng Tian

et al.

Acta Pharmacologica Sinica, Journal Year: 2025, Volume and Issue: unknown

Published: Feb. 26, 2025

Abstract Neuroinflammation is crucial for the pathogenesis of major depression. Preclinical studies have shown potential anti-inflammatory agents, specifically costunolide (COS), correlate with antidepressant effects. In this study, we investigated molecular mechanisms underlying actions COS. Chronic restraint stress (CRS) was induced in male mice. The mice were treated either intra-DG injection COS (5 μM, 1 μL per side) or (20 mg/kg, i.p.) week. We showed that administration through both routes significantly ameliorated depressive-like behavior CRS-exposed Furthermore, improved chronic stress-induced adult hippocampal neurogenesis deficits attenuating microglia-derived neuroinflammation. demonstrated μM) exerted anti-neuroinflammatory effects LPS-treated BV2 cells via inhibiting microglial Akt/mTOR/NF-κB pathway; inactivation mTOR/NF-κB/IL-1β pathway required pro-neurogenic action Our results reveal mechanism normalizing neuroinflammation to improve deficits, supporting agents as a therapeutic strategy

Language: Английский

Citations

1

Assessment of CRISPRa-mediated gdnf overexpression in an In vitro Parkinson’s disease model DOI Creative Commons
Paula Guzmán-Sastoque,

Sebastián Sotelo,

Natalia P. Esmeral

et al.

Frontiers in Bioengineering and Biotechnology, Journal Year: 2024, Volume and Issue: 12

Published: Aug. 8, 2024

Introduction Parkinson’s disease (PD) presents a significant challenge in medical science, as current treatments are limited to symptom management and often carry side effects. Our study introduces an innovative approach evaluate the effects of gdnf overexpression mediated by CRISPRa vitro model disease. The expression can have neuroprotective effects, being related modulation neuroinflammation pathways associated with cell survival, differentiation, growth. Methods We developed targeted delivery system using magnetite nanostructured vehicle for efficient transport genetic material. This has resulted substantial increase, up 200-fold) In mixed primary culture astrocytes, neurons, microglia. Results Discussion exhibits endosomal escape more than 56%, crucial effective activation material within cells. increased correlates notable reduction MAO-B complex activity, reaching basal values 14.8 μU/μg protein, reactive oxygen species. Additionally, there is 34.6% increase viability treated neurotoxin MPTP. shows that increasing remediate some cellular symptoms novel system.

Language: Английский

Citations

5

Cordycepin alleviates renal ischemia-reperfusion injury by suppressing the p38/JNK signaling pathway DOI
Qi Chen, Jiayu Guo, Shangting Han

et al.

International Immunopharmacology, Journal Year: 2025, Volume and Issue: 150, P. 114264 - 114264

Published: Feb. 15, 2025

Language: Английский

Citations

0

Cordycepin Ameliorates Kainic Acid‐Induced HT22 Cell Neurotoxicity by Activating GPR120‐Mediated Mitophagy DOI Open Access

YONG-ZHI SAN,

Minghua Wang

Developmental Neurobiology, Journal Year: 2025, Volume and Issue: 85(2)

Published: Feb. 25, 2025

Mitophagy is important for normal neural activity. Epilepsy intimately linked to neurotoxicity due mitochondrial dysfunction. Cordycepin (Cor) has been shown exert neuroprotective effects. This study aims investigate whether Cor could mitigate in epilepsy by modulating mitophagy. In vitro, kainic acid (KA) was utilized induce cytotoxicity HT22 cell. Cell viability assessed using the CCK-8 assay, while cell damage evaluated through an LDH kit. Flow cytometry used assess apoptosis. The expressions of G protein-coupled receptor 120 (GPR120), apoptosis, and mitophagy-related proteins were analyzed western blot. Inflammatory factors oxidative stress levels examined kits. DCFH-DA staining applied observe cellular reactive oxygen species (ROS) levels. three-dimensional coordinates GPR120 retrieved from PDB database, molecular docking performed AutoDock. Immunofluorescence mitophagy level. significantly attenuated KA-induced injury inflammation, suppressing ROS Notably, ameliorated decrease level observed cells treated with KA. expression upregulated following KA treatment further elevated after adding Cor. bind GPR120. Interference reversed ameliorative effects on cells. Overall, alleviated neurotoxic stress. protective effect may be mediated GPR120-regulated

Language: Английский

Citations

0

Quercetin protects against neuronal toxicity by activating the PI3K/Akt/GSK-3β pathway in vivo models of MPTP-induced Parkinson’s disease DOI Creative Commons
Y. Li,

Minghao Man,

Yiyuan Tian

et al.

Inflammopharmacology, Journal Year: 2025, Volume and Issue: unknown

Published: March 27, 2025

Quercetin is a flavonoid commonly found in various fruits, vegetables, and grains. Studies have demonstrated that quercetin may help protect neuronal cells from damage caused by neurotoxins associated with Parkinson's disease, however, the underlying mechanism remains unclear. The current study aimed to investigate neuroprotective effects of MPTP-induced disease mouse models elucidate its mechanistic role modulating PI3K/Akt/GSK-3β signaling pathway. Male C57BL/6 mice were divided into control, MPTP, quercetin, MPTP + groups. protective on evaluated using animal behaviour analysis, histopathological examination, immunofluorescence staining. Subsequently, network pharmacology was utilized determine primary target sites disease. Finally, western blotting molecular docking techniques applied validate identified targets. significantly improved motor deficits mice, reduced atrophy, preserved TH+ dopaminergic neurons. Western analysis revealed upregulated anti-inflammatory IL-10 (p < 0.01) TGF-β while suppressing pro-inflammatory IL-1β iNOS 0.01). It activated pathway increasing phosphorylation PI3K 0.01), Akt GSK-3β also elevated anti-apoptotic Bcl-2 pro-apoptotic Bax Caspase-9 Molecular confirmed strong binding between (binding energies: -6.44 -5.24 kcal/mol). alleviates pathology inhibiting neuroinflammation, reducing apoptosis, activating These findings underscore potential as multi-target therapeutic agent for

Language: Английский

Citations

0

Rilmenidine attenuates intracerebral hemorrhage by regulating autophagy flux and apoptosis via the HO-1/Fe2+/ERK pathway DOI

Qiuwei Hua,

Minghui Lu,

Zhiyang Li

et al.

Neuroscience, Journal Year: 2025, Volume and Issue: unknown

Published: March 1, 2025

Language: Английский

Citations

0

Exploring Cordycepin as a Neuroprotective Agent in Huntington's Disease: In Vitro and In Vivo Insights DOI Creative Commons
Chih‐Wei Tung,

Siew Chin Chan,

Pei‐Hsun Cheng

et al.

Pharmacology Research & Perspectives, Journal Year: 2025, Volume and Issue: 13(2)

Published: April 1, 2025

ABSTRACT Huntington's disease (HD) is a challenging neurodegenerative disorder linked to Huntingtin ( HTT ) gene mutation, lacking an effective cure despite numerous therapeutic attempts. Cordyceps sinensis , recognized for its health benefits, particularly constituent cordycepin, exhibits neuroprotective effects in various diseases. However, the potential of cordycepin HD remains insufficiently explored. In this study, vitro experiments using cell models demonstrate that treatment enhances survival, slightly diminishes mutant aggregates, and improves neuronal formation. vivo investigations on R6/2 transgenic mice reveal modest increase body weight slight amelioration pathological aggregates following administration, although behavioral changes are not significant. While underlying mechanisms remain unexplored, findings suggest cordycepin's promise as supplementary HD, providing reducing protein aggregates.

Language: Английский

Citations

0

Clinical study to investigate the adjuvant role of Pentoxifylline in patients with Parkinson's disease: A randomized controlled study DOI

Mohannad O Khrieba,

Sahar K. Hegazy,

Wessam Fathi Mohammed

et al.

International Immunopharmacology, Journal Year: 2025, Volume and Issue: 156, P. 114689 - 114689

Published: April 19, 2025

Language: Английский

Citations

0

S100A8 knockdown activates the PI3K/AKT signaling pathway to inhibit microglial autophagy and improve cognitive impairment mediated by chronic sleep deprivation DOI Creative Commons
Yanhong Xiong,

Weidong Liang,

Xifeng Wang

et al.

International Immunopharmacology, Journal Year: 2024, Volume and Issue: 143, P. 113375 - 113375

Published: Oct. 16, 2024

Cognitive dysfunction is one of the major symptoms chronic sleep deprivation (CSD). Abnormal autophagy and apoptosis are thought to be important mechanisms. S100 Calcium Binding Protein A8 (S100A8) plays a key role in microglia. This study investigated whether S100A8 knockdown can effectively inhibit aberrant microglia improve cognitive function by activating phosphatidylinositol 3-kinase (PI3K)/protein kinase B (AKT) signaling pathway under CSD conditions.

Language: Английский

Citations

0