The Mitochondria‐Targeted Micelle Inhibits Alzheimer's Disease Progression by Alleviating Neuronal Mitochondrial Dysfunction and Neuroinflammation DOI Open Access
Wenqiang Qian,

Daozhou Liu,

Jie Liu

et al.

Small, Journal Year: 2024, Volume and Issue: unknown

Published: Dec. 23, 2024

Mitochondrial dysfunction plays an important role in neuroinflammation and cognitive impairment Alzheimer's disease (AD). Herein, this work designs a mitochondria-targeted micelle CsA-TK-SS-31 (CTS) to block the progression of AD by simultaneously alleviating mitochondrial microglia neurons. The peptide SS-31 drives cyclosporin A (CsA) penetrate blood-brain barrier (BBB) delivers CsA mitochondria neurons brains 5 × FAD mice. Under high level reactive oxygen species (ROS) environment damaged neurons, linker (thioketal, TK) between is broken are released while consuming ROS microenvironment. synergistically restore membrane potential balance fission fusion mitochondria, which subsequently protect from apoptosis reduce activation Ultimately, mice ameliorated. This research provides synergistic treatment strategy for through function simultaneously.

Language: Английский

Inhibition SIRT1 to regulate FOXP3 or RORγt can restore the balance of Treg/Th17 axis in ulcerative colitis and enhance the anti-inflammatory effect of moxibustion DOI Creative Commons
Yuanbing Zhu, Yuemei Wang,

Xiaotong Zuo

et al.

Frontiers in Immunology, Journal Year: 2025, Volume and Issue: 15

Published: Jan. 10, 2025

Ulcerative colitis (UC) is a chronic inflammatory disease. Patients with UC typically exhibit disruption of the Treg/Th17 immune axis, but its exact mechanism still unclear. This study first analyzed RNA- seq data from public databases humans and mice, in vitro cytology experiments were conducted to induce or inhibit expression SIRT1. In vivo, mice treated moxibustion SIRT1 inhibitor EX-527 confirm changes transcription factors identified through analysis datasets. The results show that axis an important feature UC. Differential gene infiltration showed upstream factors, including Forkhead box P3 (FOXP3), significantly disrupted. experiments, indicate activated LPS induced inflammation, subsequently perturbing balance axis. Finally, vivo studies, have shown administering leads increasing FOXP3 decreasing RORγt colon tissue. addition, traditional Chinese can down regulate SIRT1, directly affecting Th17/Treg combined use further improves therapeutic effect moxibustion. Our research shows inhibition Treg Th17 finding indicates new potential target for treatment

Language: Английский

Citations

0
Direct Inhibition of Macrophage STING Signaling by Curcumol Protects Against Myocardial Infarction via Attenuating the Inflammatory Response DOI
Na Yang,

Guanye Yu,

Tianhao Liu

et al.

Phytomedicine, Journal Year: 2025, Volume and Issue: 138, P. 156403 - 156403

Published: Jan. 18, 2025

Language: Английский

Citations

0
Carboxymethyl chitosan oligosaccharide prevents the progression of chronic kidney disease as a Nrf2-dependent apoptosis inhibitor DOI Creative Commons

Xiaozheng Yuan,

Huan He,

Youtao Xu

et al.

Carbohydrate Polymer Technologies and Applications, Journal Year: 2025, Volume and Issue: unknown, P. 100728 - 100728

Published: Feb. 1, 2025

Language: Английский

Citations

0
Curcumol Ameliorates Cisplatin-induced Nephrotoxicity by Targeting TAK1 and Inhibiting MAPK and NF-κB Pathways DOI

Xuejin Jin,

Yuan Miao,

Lingkun Wang

et al.

Phytomedicine, Journal Year: 2025, Volume and Issue: unknown, P. 156752 - 156752

Published: April 1, 2025

Language: Английский

Citations

0
The Aging Immune System: A Critical Attack on Ischemic Stroke DOI

Wenzhe Xu,

Yuying Guo,

Linna Zhao

et al.

Molecular Neurobiology, Journal Year: 2024, Volume and Issue: unknown

Published: Sept. 14, 2024

Language: Английский

Citations

2
ACTH-like Peptides Compensate Rat Brain Gene Expression Profile Disrupted by Ischemia a Day After Experimental Stroke DOI Creative Commons
Ivan B. Filippenkov, Yana Yu. Shpetko, Vasily Stavchansky

et al.

Biomedicines, Journal Year: 2024, Volume and Issue: 12(12), P. 2830 - 2830

Published: Dec. 13, 2024

Background: Ischemic stroke results from a disruption of cerebral blood flow. Adrenocorticotropic hormone (ACTH) serves as the basis for creation synthetic peptides neuroprotective agents therapy. Previously, using RNA-Seq we first revealed differential expressed genes (DEGs) associated with ACTH(4–7)PGP (Semax) and ACTH(6–9)PGP under ischemia conditions. Analysis was carried out at 4.5 h after transient middle artery occlusion (tMCAO) model in ipsilateral frontal cortex rat brain. Methods: Here, analyzed penumbra-associated rats actions same 24 tMCAO RNA-Seq. Results: 3774 DEGs (fold change > 1.5 Padj < 0.05) were identified conditions, whereas 1539 2066 Semax tMCAO. Furthermore, both significantly reduced expression distortions caused by 1171 immune neurosignaling pathways. Concomitantly, there 32 versus administration Besides, neurogenesis-, angiogenesis-, protein kinase- growth factor-related action. observed effect histological level brains Thus, here demonstrate transcriptome manifestation this effect. comparison previous data post-tMCAO time point showed that pattern peptide action on depends elapsed Conclusions: We more similar to than different it day At point, ACTH-like compensated brain gene profiles disrupted ischemia. our may be useful selecting effective structures future anti-stroke drugs appropriate post-stroke points their testing.

Language: Английский

Citations

1
The Mitochondria‐Targeted Micelle Inhibits Alzheimer's Disease Progression by Alleviating Neuronal Mitochondrial Dysfunction and Neuroinflammation DOI Open Access
Wenqiang Qian,

Daozhou Liu,

Jie Liu

et al.

Small, Journal Year: 2024, Volume and Issue: unknown

Published: Dec. 23, 2024

Mitochondrial dysfunction plays an important role in neuroinflammation and cognitive impairment Alzheimer's disease (AD). Herein, this work designs a mitochondria-targeted micelle CsA-TK-SS-31 (CTS) to block the progression of AD by simultaneously alleviating mitochondrial microglia neurons. The peptide SS-31 drives cyclosporin A (CsA) penetrate blood-brain barrier (BBB) delivers CsA mitochondria neurons brains 5 × FAD mice. Under high level reactive oxygen species (ROS) environment damaged neurons, linker (thioketal, TK) between is broken are released while consuming ROS microenvironment. synergistically restore membrane potential balance fission fusion mitochondria, which subsequently protect from apoptosis reduce activation Ultimately, mice ameliorated. This research provides synergistic treatment strategy for through function simultaneously.

Language: Английский

Citations

0