Ginsenoside Rb3 Promotes Opa1‐Mediated Regenerative Neurogenesis via Activating the Ido1 Pathway in Ischemic Stroke DOI
Lei Wang, Na Qin,

Shiman Gao

et al.

Phytotherapy Research, Journal Year: 2024, Volume and Issue: unknown

Published: Nov. 21, 2024

ABSTRACT The activation of neural stem cells (NSCs) residing in the subventricular zone (SVZ) and dentate gyrus (DG) has been shown to promote restoration damaged brain tissues. Ginsenoside Rb3 (Rb3) is a bioactive substance known for its pharmacological properties treating neurological disorders. This study investigated effects on regeneration following ischaemic stroke (IS) underlying mechanisms involved. Male C57BL/6 mice were utilized subjected middle cerebral artery occlusion/reperfusion (MCAO/R). Post‐ischemia, was administered through intraperitoneal (i.p.) injection either 7 or 28 days. promotion regenerative neurogenesis detected by immunofluorescence staining. NSCs pretreated with different concentrations 24 h before oxygen–glucose deprivation/reoxygenation (OGD/R) exposure. Afterward, staining flow cytometry used detect migration proliferation OGD/R‐induced NSCs. Furthermore, Adeno‐associated virus (AAV) transduction experiments, siRNA transfection gene knockout targeted metabolomics analysis, molecular dynamics simulation, cellular thermal shift assay (CETSA), drug affinity responsive target stability (DARTS) assays explore mechanism IS. promoted Opa1‐mediated proliferation. Knockdown Opa1 blunted above‐promoting both brains ischemia–reperfusion (I/R)‐treated OGD/R‐treated Mechanistically, metabolomics, dynamics, docking, CETAS, DARTS experiments showed that required Ido1 served as direct repair I/R injury. Moreover, studies siRNA‐mediated knockdown KO revealed inhibition attenuated enhancing effect mitochondrial fusion. Our provides novel evidence promotes an Ido1/Opa1‐mediated pathway involving interaction between Ido1, leading improved long‐term function. These results indicate other fusion promoters could be potential neurorestorative strategy

Language: Английский

Extracellular cold-inducible RNA-binding protein in CNS injury: molecular insights and therapeutic approaches DOI Creative Commons

Dmitriy Lapin,

Archna Sharma, Ping Wang

et al.

Journal of Neuroinflammation, Journal Year: 2025, Volume and Issue: 22(1)

Published: Jan. 21, 2025

Abstract Central nervous system (CNS) injuries, such as ischemic stroke (IS), intracerebral hemorrhage (ICH) and traumatic brain injury (TBI), are a significant global burden. The complex pathophysiology of CNS is comprised primary secondary injury. Inflammatory incited by damage-associated molecular patterns (DAMPs) which signal variety resident cells infiltrating immune cells. Extracellular cold-inducible RNA-binding protein (eCIRP) DAMP acts through multiple non-immune to promote inflammation. Despite the well-established role eCIRP in systemic sterile inflammation, its less elucidated. Recent literature suggests that pleiotropic inflammatory mediator also being evaluated clinical biomarker indicate prognosis injuries. This review provides broad overview injury, with focus on immune-mediated neuroinflammation. We then what known about mechanisms both non-CNS cells, identifying opportunities for further study. explore eCIRP’s potential prognostic marker severity outcome. Next, we provide an eCIRP-targeting therapeutics suggest strategies develop these agents ameliorate Finally, emphasize exploring novel mechanisms, aside from neuroinflammation, critical therapeutic target

Language: Английский

Citations

2

Role of efferocytosis in chronic pain —— From molecular perspective DOI Creative Commons

Hu Zang,

Xiaoyu Ji, Wenlong Yao

et al.

Neurobiology of Disease, Journal Year: 2025, Volume and Issue: 207, P. 106857 - 106857

Published: Feb. 25, 2025

Language: Английский

Citations

0

Unveiling the neuroprotection effects of Volvalerenic acid A: Mitochondrial fusion induction via IDO1-mediated Stat3-Opa1 signaling pathway DOI

Shanchun Ge,

Lei Wang,

Chang Jin

et al.

Phytomedicine, Journal Year: 2024, Volume and Issue: 129, P. 155555 - 155555

Published: March 20, 2024

Language: Английский

Citations

1

Notoginseng leaf triterpenes promotes angiogenesis by activating the Nrf2 pathway and AMPK/SIRT1-mediated PGC-1/ERα axis in ischemic stroke DOI
Lei Wang, Na Qin,

Shanchun Ge

et al.

Fitoterapia, Journal Year: 2024, Volume and Issue: 176, P. 106045 - 106045

Published: May 31, 2024

Language: Английский

Citations

1

Gut Microbiota and Tryptophan Metabolism in Pathogenesis of Ischemic Stroke: A Potential Role for Food Homologous Plants DOI Open Access
Lei Wang, Na Qin,

Liuliu Shi

et al.

Molecular Nutrition & Food Research, Journal Year: 2024, Volume and Issue: 68(23)

Published: Nov. 17, 2024

The intestinal flora is involved in the maintenance of human health and development diseases, closely related to brain. As an essential amino acid, tryptophan (TRP) participates a variety physiological functions body affects growth body. TRP catabolites produced by gut microbiota are important signaling molecules for microbial communities host-microbe interactions, play role maintaining disease pathogenesis. review first demonstrates evidence metabolism stroke relationship between metabolism. Furthermore, reveals that food homologous plants (FHP) bioactive compounds have been shown regulate various metabolic pathways microbiota, including biosynthesis valine, leucine, isoleucine, vitamin B6 most notable alteration interaction offers plausible explanation bioactivities FHP treatment ischemic (IS). This enhances comprehension underlying mechanisms associated with bioactivity on IS.

Language: Английский

Citations

1

Efferocytosis: the resolution of inflammation in cardiovascular and cerebrovascular disease DOI Creative Commons
Bingtao Zhang,

Yan Zou,

Z. Y. Yuan

et al.

Frontiers in Immunology, Journal Year: 2024, Volume and Issue: 15

Published: Nov. 26, 2024

Cardiovascular and cerebrovascular diseases have surpassed cancer as significant global health challenges, which mainly include atherosclerosis, myocardial infarction, hemorrhagic stroke ischemia stroke. The inflammatory response immediately following these profoundly impacts patient prognosis recovery. Efficient resolution of inflammation is crucial not only for halting the process but also restoring tissue homeostasis. Efferocytosis, phagocytic clearance dying cells by phagocytes, especially microglia macrophages, plays a critical role in this process. Upon injury, phagocytes are recruited to site damage where they engulf clear through efferocytosis. Efferocytosis suppresses secretion pro-inflammatory cytokines, stimulates production anti-inflammatory modulates phenotype accelerates inflammation, promotes repair. It involves three main stages: recognition, engulfment, degradation cells. Optimal removal apoptotic cargo requires finely tuned machinery associated modifications. Key molecules efferocytosis, such 'Find-me signals', 'Eat-me 'Don't eat-me been shown enhance efferocytosis cardiovascular diseases. Moreover, various additional molecules, pathways, mitochondrial metabolic processes identified outcomes via diverse experimental models. Impaired can lead inflammation-associated pathologies prolonged recovery periods. Therefore, review consolidates current understanding mechanisms its application diseases, proposing future research directions.

Language: Английский

Citations

1

Therapeutic implication of targeting mitochondrial drugs designed for efferocytosis dysfunction DOI
Wan-Ting Liu,

Chao-Quan Li,

Ao-Ni Fu

et al.

Journal of drug targeting, Journal Year: 2024, Volume and Issue: 32(10), P. 1169 - 1185

Published: Aug. 5, 2024

Efferocytosis refers to the process by which phagocytes remove apoptotic cells and related products. It is essential for growth development of body, repair damaged or inflamed tissues, balance immune system. Damaged efferocytosis will cause a variety chronic inflammation system diseases. Many studies show that mediated mitochondria. Mitochondrial metabolism, mitochondrial dynamics, communication between mitochondria other organelles can all affect phagocytes' clearance cells. Therefore, targeting modulate phagocyte an anticipated strategy prevent treat inflammatory diseases autoimmune In this review, we introduced mechanism pivoted role in efferocytosis. addition, focused on therapeutic implication drugs dysfunction.

Language: Английский

Citations

0

Ginsenoside Rb3 Promotes Opa1‐Mediated Regenerative Neurogenesis via Activating the Ido1 Pathway in Ischemic Stroke DOI
Lei Wang, Na Qin,

Shiman Gao

et al.

Phytotherapy Research, Journal Year: 2024, Volume and Issue: unknown

Published: Nov. 21, 2024

ABSTRACT The activation of neural stem cells (NSCs) residing in the subventricular zone (SVZ) and dentate gyrus (DG) has been shown to promote restoration damaged brain tissues. Ginsenoside Rb3 (Rb3) is a bioactive substance known for its pharmacological properties treating neurological disorders. This study investigated effects on regeneration following ischaemic stroke (IS) underlying mechanisms involved. Male C57BL/6 mice were utilized subjected middle cerebral artery occlusion/reperfusion (MCAO/R). Post‐ischemia, was administered through intraperitoneal (i.p.) injection either 7 or 28 days. promotion regenerative neurogenesis detected by immunofluorescence staining. NSCs pretreated with different concentrations 24 h before oxygen–glucose deprivation/reoxygenation (OGD/R) exposure. Afterward, staining flow cytometry used detect migration proliferation OGD/R‐induced NSCs. Furthermore, Adeno‐associated virus (AAV) transduction experiments, siRNA transfection gene knockout targeted metabolomics analysis, molecular dynamics simulation, cellular thermal shift assay (CETSA), drug affinity responsive target stability (DARTS) assays explore mechanism IS. promoted Opa1‐mediated proliferation. Knockdown Opa1 blunted above‐promoting both brains ischemia–reperfusion (I/R)‐treated OGD/R‐treated Mechanistically, metabolomics, dynamics, docking, CETAS, DARTS experiments showed that required Ido1 served as direct repair I/R injury. Moreover, studies siRNA‐mediated knockdown KO revealed inhibition attenuated enhancing effect mitochondrial fusion. Our provides novel evidence promotes an Ido1/Opa1‐mediated pathway involving interaction between Ido1, leading improved long‐term function. These results indicate other fusion promoters could be potential neurorestorative strategy

Language: Английский

Citations

0