Pantothenic acid-mediated inhibition of microglial inflammation via the JAK2/STAT3 pathway enhances motor function recovery after Spinal cord injury DOI Creative Commons

Yuepeng Fang,

Ce Zhang,

Zhijie Yang

et al.

Research Square (Research Square), Journal Year: 2024, Volume and Issue: unknown

Published: Dec. 19, 2024

Abstract This study employed transcriptome sequencing and targeted metabolomics to delve into the molecular alterations in mouse spinal cords following cord injury (SCI). Notably, a significant depletion of pantothenic acid (PA) was observed injured cord, exhibiting an inverse correlation with microglial inflammation activation. To further elucidate this relationship, experimental interventions using PA were conducted SCI models. The results demonstrated that administration effectively inhibited via modulation JAK2/STAT3 signaling pathway. inhibition not only mitigated neuroinflammatory milieu but also fostered environment conducive axonal growth neuronal regeneration. Consequently, mice treated exhibited improved motor function recovery compared untreated controls. Our findings deepen understanding relationship between processes highlight therapeutic potential promoting regeneration functional recovery.

Language: Английский

Modulating Neuroinflammation as a Prospective Therapeutic Target in Alzheimer’s Disease DOI Creative Commons

Eunshil Lee,

Yongmin Chang

Cells, Journal Year: 2025, Volume and Issue: 14(3), P. 168 - 168

Published: Jan. 22, 2025

The recent approval of lecanemab highlights that the amyloid beta (Aβ) protein is an important pathological target in Alzheimer’s disease (AD) and further emphasizes significance neuroinflammatory pathways regulating Aβ accumulation. Indeed, accumulation triggers microglia activation, which are key mediators neuroinflammation. inflammatory responses this process can lead to neuronal damage functional decline. Microglia secrete proinflammatory cytokines accelerate death release anti-inflammatory growth factors contributing recovery protection. Thus, play a dual role neurodegeneration neuroprotection, complicating their function AD. Therefore, elucidating complex interactions between protein, microglia, neuroinflammation essential for developing new strategies treating This review investigates receptors involved activating aims enhance understanding how these processes impact AD, as well they be regulated. also analyzed studies reported existing literature ongoing clinical trials. Overall, will contribute regulatory mechanisms therapies slow progression

Language: Английский

Citations

1
Pharmacological mechanisms of puerarin in the treatment of Parkinson's disease: An overview DOI Open Access
Nianping Zhang, Peng Guo, Yan Zhao

et al.

Biomedicine & Pharmacotherapy, Journal Year: 2024, Volume and Issue: 177, P. 117101 - 117101

Published: July 14, 2024

Puerarin, a monomer of traditional Chinese medicine, is key component Pueraria radix. Both clinical and experimental researches demonstrated that puerarin has therapeutic effects on Parkinson's disease (PD). Puerarin's pharmacological mechanisms include: 1) Anti-apoptosis. Puerarin inhibits cell apoptosis through the phosphatidylinositol-4,5-bisphosphate 3-kinase (PI3K)/protein kinase B (Akt) c-Jun N-terminal (JNK) signaling pathways. also exerts hormone-like effect against apoptosis; 2) Anti-oxidative stress injury. Nrf2 nuclear exclusion GSK-3β/Fyn pathway to promote accumulation in nucleus, then promotes antioxidant synthesis Nrf2/ARE protect oxidative stress; 3) Neuroprotective by intervening ubiquitin-proteasome system (UPS) autophagy-lysosomal (ALP). significantly enhances activity chaperone-mediated autophagy (CMA), which downregulates expression α-synuclein, reduces its accumulation, thus improves function damaged neurons. Additionally, increases proteasome decreases ubiquitin-binding proteins, thereby preventing toxic intracellular proteins; 4) Alleviating inflammatory response. conversion microglia M1 phenotype while inducing transition M2 phenotype. Furthermore, secretion anti-inflammatory factor pro-inflammatory factors; 5) Increasing levels dopamine metabolites. could increase dopamine, homovanillic acid (HVA) 3,4-dihydroxyphenylacetic (DOPAC) striatum; 6) Promoting neurotrophic neuronal repair. glial cell-derived (GDNF), brain-derived (BDNF) nerve growth (NGF), exerting neuroprotective effect. Moreover, regulation gut microbiota may be potential mechanism for treatment PD. The current review discusses molecular puerarin, provide insight into active components medicine

Language: Английский

Citations

5
Investigating the Potential Therapeutic Targeting of the JAK-STAT Pathway in Cerebrovascular Diseases: Opportunities and Challenges DOI
Jiawei Wu, Bingxin Wang,

Li-Ping Shen

et al.

Molecular Neurobiology, Journal Year: 2025, Volume and Issue: unknown

Published: March 18, 2025

Language: Английский

Citations

0
Tofacitinib prevents depressive-like behaviors through decreased hippocampal microgliosis and increased BDNF levels in both LPS-induced and CSDS-induced mice DOI
Yanan Gao,

Kaijun Pan,

Yong-Mei Zhang

et al.

Acta Pharmacologica Sinica, Journal Year: 2024, Volume and Issue: unknown

Published: Sept. 30, 2024

Language: Английский

Citations

2
Testing the Simplified Molecular Dynamics Approach to Improve the Reproduction of ECD Spectra and Monitor Aggregation DOI Open Access
Attila Mándi,

Aliz Rimóczi,

Andrea Vasas

et al.

International Journal of Molecular Sciences, Journal Year: 2024, Volume and Issue: 25(12), P. 6453 - 6453

Published: June 12, 2024

A simplified molecular-dynamics-based electronic circular dichroism (ECD) approach was tested on three condensed derivatives with limited conformational flexibility and an isochroman-2H-chromene hybrid, the ECD spectra of which could not be precisely reproduced by conventional calculation protocol. Application explicit solvent molecules at molecular mechanics (MD) level in dynamics simulations subsequent TDDFT-ECD for unoptimized MD structures able to improve agreements between experimental computed spectra. Since enhancements were achieved even flexibility, deformations caused multitudes conformers produced geometries seem key factors better agreement. The confirm that aggregation phenanthrene natural product luzulin had a significant contribution specific wavelength range ECD. has proved dimer formation occurred solution this responsible anomalous spectrum. scope limitations method have also been discussed.

Language: Английский

Citations

0
Heme oxygenase-1: potential therapeutic targets for periodontitis DOI Creative Commons

Weiwei Lv,

Si-Yuan Hu, Fei Yang

et al.

PeerJ, Journal Year: 2024, Volume and Issue: 12, P. e18237 - e18237

Published: Oct. 15, 2024

Periodontitis is one of the most prevalent inflammatory disease worldwide, which affects 11% global population and a major cause tooth loss. Recently, oxidative stress (OS) has been found to be pivital pathophysiological mechanism periodontitis, overactivated OS will lead inflammation, apoptosis, pyroptosis alveolar bone resorption. Interestingly, heme oxygenase-1 (HO-1), rate-limiting enzyme in degradation, can exert antioxidant activites through its products-carbon monoxide (CO), Fe

Language: Английский

Citations

0
Pantothenic acid-mediated inhibition of microglial inflammation via the JAK2/STAT3 pathway enhances motor function recovery after Spinal cord injury DOI Creative Commons

Yuepeng Fang,

Ce Zhang,

Zhijie Yang

et al.

Research Square (Research Square), Journal Year: 2024, Volume and Issue: unknown

Published: Dec. 19, 2024

Abstract This study employed transcriptome sequencing and targeted metabolomics to delve into the molecular alterations in mouse spinal cords following cord injury (SCI). Notably, a significant depletion of pantothenic acid (PA) was observed injured cord, exhibiting an inverse correlation with microglial inflammation activation. To further elucidate this relationship, experimental interventions using PA were conducted SCI models. The results demonstrated that administration effectively inhibited via modulation JAK2/STAT3 signaling pathway. inhibition not only mitigated neuroinflammatory milieu but also fostered environment conducive axonal growth neuronal regeneration. Consequently, mice treated exhibited improved motor function recovery compared untreated controls. Our findings deepen understanding relationship between processes highlight therapeutic potential promoting regeneration functional recovery.

Language: Английский

Citations

0