Utilizing network pharmacology, pharmacodynamics, molecular biology studies, and molecular docking techniques to uncover the mechanism of the Ligusticum wallichii-borneol medication combination for the treatment of ischemic stroke in rat models DOI Creative Commons

Pelser He,

Zhifeng Wang, Yang Jiao

и другие.

Research Square (Research Square), Год журнала: 2024, Номер unknown

Опубликована: Дек. 17, 2024

Abstract Objective.To use pharmacodynamics, molecular biology studies, network pharmacology, and docking to study the mechanism of action Ligusticum wallichii (known as Chuanxiong in China, CX) borneol Bingpian BP) medication pair (CXBP) for treatment ischemic stroke. Methods. The TCMSP, ETCM, SymMap databases provided effective chemical components targets CXBP, while OMIM, GeneCards, TTD, Pubmed, Web Science, CNKI, Wanfang Data, VIP Database relevant PPI maps important were created using String database, GO KEGG enrichment analyses carried out Metascape database. "Disease-Pathway-Target-Component-Drug" was constructed Cytoscape, Pymol Autodock tools used confirm docking. Rat models MCAO established, neurological scores, TTC staining Nissl's performed. Finally, key verified by enzyme-linked immunosorbent assay (ELISA), real-time fluorescence quantitative PCR, immunohistochemistry. Results.There 33 active ingredients 419 potential involving Z-6,8',7,3'-diligustilide, Cedrene,(+)- Alpha-Funebrene, POL, Dipterocarpol, Oleanolic acid, 1-Acetyl- beta-carboline, Erythrodiol, transcription factor ESR1, pro-inflammatory PRKCA, anti-inflammatory PTPN6; pathway analysis enriched 179 signaling pathways, results comprised 2911 biological processes, 398 activities, 203 cellular components. function score brain tissue infarct region significantly lower following CXBP intervention compared group, which corroborated experimental evidence; revealed that, intervention, morphology more intact there considerably vesicles infarcted area than group; By ELISA, it possible see substantial changes expression levels PTPN6, TNF-α well a considerable down-regulation IL-1β, IL-6, group. TNF-α, IL-1β markedly downregulated; PCR indicated comparison with PRKCA decreased, down-regulated, ESR1 PTPN6 increased. Immunohistochemistry group nimodipine had higher PRKCA. Conclusions.In order improve cerebral ischemia reperfusion injury, may act through Cedrene,(+)-Alpha-Funebrene, 1-Acetyl-beta-carboline, other ingredients. acts on regulate multiple pathways.

Язык: Английский

Buyang Huanwu decoction promotes gray and white matter remyelination by inhibiting Notch signaling activation in the astrocyte and microglia after ischemic stroke DOI
Man-zhong Li,

Yuming Zhuang,

Mingcong Li

и другие.

Journal of Ethnopharmacology, Год журнала: 2025, Номер unknown, С. 119440 - 119440

Опубликована: Фев. 1, 2025

Язык: Английский

Процитировано

1
Integrating network pharmacology and bioinformatics to explore and experimentally verify the regulatory effect of Buyang Huanwu decoction on glycolysis and angiogenesis after cerebral infarction DOI

Fengming Tian,

Jian Yi, Yingfei Liu

и другие.

Journal of Ethnopharmacology, Год журнала: 2023, Номер 319, С. 117218 - 117218

Опубликована: Окт. 6, 2023

Язык: Английский

Процитировано

12
Yi-Qi-Huo-Xue decoction alleviates intracerebral hemorrhage injury through inhibiting neuronal autophagy of ipsilateral cortex via BDNF/TrkB pathway DOI Creative Commons
Dan Han, Xinyue Chang, Dan Xu

и другие.

Phytomedicine, Год журнала: 2024, Номер 128, С. 155438 - 155438

Опубликована: Фев. 19, 2024

Yi-Qi-Huo-Xue Decoction (YQHXD), a traditional Chinese medicine formula, has demonstrated efficacy in the clinical treatment of intracerebral hemorrhage (ICH) for over decade. Nevertheless, precise pharmacotherapeutic compounds YQHXD capable penetrating into cerebral tissue and pharmacological underpinnings remain ambiguous. The active components rat brains was analyzed by ultra-performance liquid chromatography coupled with quadrupole time-of-flight mass spectrometry. potential targets, pathways biological progresses ameliorating ICH induced injury predicted network pharmacology. Moreover, collagenase-induced model, primary cortex neurons exposed to hemin molecular docking were applied validate mechanisms YQHXD. Eleven identified within brains. Employing Gene Ontology (GO) Kyoto Encyclopedia Genes Genomes (KEGG) databases, our investigation concentrated on roles autophagy BDNF/TrkB signaling pathway context. results revealed that alleviated neurological dysfunction, brain water content, swelling, pathological caused ICH. Meanwhile, inhibited influx autophagosome vivo, regulated neuronal TrkB/BDNF both vivo vitro. Subsequently, N-acetyl serotonin (NAS), selective TrkB agonist, employed corroborate significance this process. combination NAS did not further enhance protective rats. Additionally, outcomes analysis nine exhibited regulatory effects TrkB. Ipsilateral activated 72 h after effectively resisted ICH, which related suppression ipsilateral via pathway. This study provides novel insights therapeutic context treatment.

Язык: Английский

Процитировано

4
miRNA506 Activates Sphk1 Binding with Sirt1 to Inhibit Brain Injury After Intracerebral Hemorrhage via PI3K/AKT Signaling Pathway DOI
Tianyu Liang,

Renyang Liu,

Jinquan Liu

и другие.

Molecular Neurobiology, Год журнала: 2024, Номер unknown

Опубликована: Окт. 12, 2024

Язык: Английский

Процитировано

4
Reprogramming of regulatory T cells in inflammatory tumor microenvironment: can it become immunotherapy turning point? DOI Creative Commons
Jinming Liu, Biao Zhang, Guolin Zhang

и другие.

Frontiers in Immunology, Год журнала: 2024, Номер 15

Опубликована: Фев. 21, 2024

Overcoming the immunosuppressive tumor microenvironment and identifying widely used immunosuppressants with minimal side effects are two major challenges currently hampering cancer immunotherapy. Regulatory T cells (Tregs) present in almost all tissues play an important role preserving autoimmune tolerance tissue homeostasis. The inflammatory causes reprogramming of Tregs, resulting conversion Tregs to phenotypes. This process ultimately facilitates immune escape or progression. However, current systemic Treg depletion therapies may lead severe toxicity. Therefore, it is crucial understand mechanism develop immunotherapies that selectively target within tumors. article provides a comprehensive review potential mechanisms involved cell explores application interference pathways has shown promise reducing number tumor-associated impairing their function during immunotherapy, thereby improving anti-tumor responses. Furthermore, deeper understanding drive could reveal new molecular targets for future treatments.

Язык: Английский

Процитировано

3
Study on the synthesis, characterization, and antitumor mechanism investigation of QZQ-01115 via targeting sphingosine kinase 2 DOI

Caiyu Liu,

Yaxin Guo,

Yutong Dong

и другие.

Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease, Год журнала: 2025, Номер unknown, С. 167829 - 167829

Опубликована: Апрель 1, 2025

Язык: Английский

Процитировано

0
Remodeling the Neuroimmune Microenvironment in Retinal Ischemia‐Reperfusion Injury via Combined CRISPR/Cas9 Targeting of ACSL4 and Isorhamnetin DOI
Wen Zhang, Lin Li,

Lusheng Ma

и другие.

Advanced Functional Materials, Год журнала: 2025, Номер unknown

Опубликована: Апрель 27, 2025

Abstract Retinal ischemia‐reperfusion (RIR) injury induces oxidative stress, excitotoxicity, inflammation, and ferroptosis, which interact through complex crosstalk, forming a retinal pathological microenvironment (RPMe) that drives ganglion cell (RGC) death. Central to these processes is the dysregulation of neuroimmune (NiMe), characterized by aberrant microglial activation around RGCs immune signaling imbalances. Here, analysis single‐cell RNA sequencing, it identifies significant sphingolipid pathway in RIR‐injured microglia, crosstalks with pathways. This crosstalk disrupts NiMe homeostasis. To address this, biomimetic nanoparticle system coated precursor membranes developed. co‐delivers CRISPR/Cas9‐based Acyl‐CoA synthetase long‐chain family member 4 (ACSL4) inhibitor suppress ferroptosis isorhamnetin, natural molecule identified directly bind protein kinase A inhibit glutamatergic synapse involved stress. By targeting its PI3K/AKT ASK1/JNK/NF‐κB pathways as well RGCs, this restores balance. The membrane‐coated offers novel, synergistic, targeted therapeutic strategy for RIR‐related diseases integrating CRISPR/Cas9 technology product therapy.

Язык: Английский

Процитировано

0
Traditional, complementary, and integrative medicine in the management of ischemic stroke: a narrative review DOI Creative Commons

S. Sowmiya,

Rukaiah Fatma Begum,

L. S. Dhivya

и другие.

Frontiers in Pharmacology, Год журнала: 2025, Номер 16

Опубликована: Май 30, 2025

Ischemic stroke remains a leading cause of mortality and long-term disability worldwide, despite advancements in acute intervention rehabilitation strategies. Traditional, Complementary, Integrative Medicine (TCIM) systems; including herbal medicine, acupuncture, mind-body interventions are increasingly being explored as adjunct therapies management. This narrative review evaluates the current evidence supporting TCIM approaches for ischemic stroke, highlighting their potential neuroprotective, anti-inflammatory, antioxidant, cerebrovascular effects. Particular emphasis is placed on well-studied botanical such Salvia miltiorrhiza Bunge [Lamiaceae; Salviae miltiorrhizae radix et rhizoma], Ginkgo biloba L. [Ginkgoaceae; folium], Panax ginseng C.A. Mey. [Araliaceae; Ginseng radix]. The discusses mechanisms action, clinical trial outcomes, integration challenges, while underscoring need standardization, quality control, rigorous scientific validation. work aims to support informed decisions regarding evidence-based practices into conventional care protocols.

Язык: Английский

Процитировано

0
Sphk1/S1P pathway promotes blood-brain barrier breakdown after intracerebral hemorrhage through inducing Nlrp3-mediated endothelial cell pyroptosis DOI Creative Commons
Mengzhao Feng, Yuan An,

Qi Qin

и другие.

Cell Death and Disease, Год журнала: 2024, Номер 15(12)

Опубликована: Дек. 23, 2024

Abstract Intracerebral hemorrhage (ICH) is a severe stroke subtype with high mortality and limited therapeutic options. The blood-brain barrier (BBB) breakdown post-ICH exacerbates secondary brain injury, highlighting the need for targeted therapies to preserve BBB integrity. We aim investigate role of Sphk1/S1P pathway in following ICH evaluate potential Sphk1 inhibition mitigating this breakdown. Using combination human patient samples, mouse models ICH, vitro cellular assays, we assessed expression levels after changes ICH. inhibitor PF543 siRNAs were utilized explore pathway’s impact on integrity underlying mechanisms. results indicate significant upregulation peri-hematomal tissue which correlates increased leakage. Pharmacological attenuates leakage, reduces hematoma volume, improves neurological outcomes mice. At molecular ultrastructural level, protects by preserving tight junction proteins suppressing endothelial transcytosis. Furthermore, mechanistic studies reveal that promotes Nlrp3-mediated pyroptosis cells through ERK1/2 signaling pathway. Taken together, plays critical ICH-induced breakdown, its represents promising strategy management.

Язык: Английский

Процитировано

3
FABP3 Induces Mitochondrial Autophagy to Promote Neuronal Cell Apoptosis in Brain Ischemia-Reperfusion Injury DOI
Fangfang Zhong, Bo Wei,

Guo-Xiang Bao

и другие.

Neurotoxicity Research, Год журнала: 2024, Номер 42(4)

Опубликована: Июль 15, 2024

Язык: Английский

Процитировано

2