Vitexin Suppresses High-Glucose-upregulated Adhesion Molecule Expression in Endothelial Cells through Inhibiting NF-κB Signaling Pathway

ACS Omega, Год журнала: 2024, Номер unknown

Опубликована: Июль 21, 2024

Vascular damage is one of the significant complications diabetes mellitus (DM). Central to this endothelial damage, especially under high-glucose conditions, which promotes inflammation via NF-κB signaling pathway. Inflammatory processes in cells directly contribute dysfunction, such as promoting inflammatory cytokine release and activation adhesion molecules. Vitexin, a compound found many medicinal plants, shows promise countering oxidative stress diabetic contexts modulating blood glucose. However, its effect on high-glucose-induced cell has not yet been studied. This research explores vitexin's potential role process, focusing influence pathway cells. Human umbilical vein (HUVECs) were stimulated with 30 mM glucose (high glucose, HG) or without vitexin treatment for 24 h. Western blotting assay was conducted p-p38. Adhesion molecules (ICAM-1, VCAM-1, E-selectin, MCP-1) studied using flow cytometry, while pro-inflammatory cytokines investigated ELISA. Monocyte vascular permeability tests confirm protective HG exposure. study confirms capacity suppress p38 MAPK reducing HG-elevated secretion. Additionally, mitigates HG-stimulated monocyte adhesion. In conclusion, therapeutic against hyperglycemia-related MAPK/NF-κB inhibition.

Язык: Английский

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Progress in the study of anti-tumor effects and mechanisms of vitexin

Pharmacological Reports, Год журнала: 2024, Номер unknown

Опубликована: Окт. 31, 2024

Язык: Английский

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Advances in the study of key cells and signaling pathways in renal fibrosis and the interventional role of Chinese medicines

Frontiers in Pharmacology, Год журнала: 2024, Номер 15

Опубликована: Дек. 2, 2024

Renal fibrosis (RF) is a pathological process characterized by the excessive accumulation of extracellular matrix (ECM), which triggers repair cascade in response to stimuli and pathogenic factors, leading activation molecular signaling pathways involved fibrosis. This article discusses key cells, molecules, implicated pathogenesis RF, with particular focus on tubular epithelial cells (TECs), cellular senescence, ferroptosis, autophagy, epithelial-mesenchymal transition (EMT), transforming growth factor-β(TGF-β)/Smad signaling. These factors drive core regulatory that significantly influence RF. A comprehensive understanding their roles essential. Through literature review, we explore recent advancements traditional Chinese medicine (TCM) aimed at reducing RF inhibiting chronic kidney disease (CKD). We summarize, analyze, elaborate important role herbs aiming provide new directions for application prevention treatment, as well scientific guidance clinical practices.

Язык: Английский

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Targeting programmed cell death in diabetic kidney disease: from molecular mechanisms to pharmacotherapy

Molecular Medicine, Год журнала: 2024, Номер 30(1)

Опубликована: Дек. 20, 2024

Abstract Diabetic kidney disease (DKD), one of the most prevalent microvascular complications diabetes, arises from dysregulated glucose and lipid metabolism induced by hyperglycemia, resulting in deterioration renal cells such as podocytes tubular epithelial cells. Programmed cell death (PCD), comprising apoptosis, autophagy, ferroptosis, pyroptosis, necroptosis, represents a spectrum demise processes intricately governed genetic mechanisms vivo. Under physiological conditions, PCD facilitates turnover cellular populations serves protective mechanism to eliminate impaired or cells, thereby preserving tissue homeostasis amidst hyperglycemic stress. However, existing research predominantly elucidates individual modes death, neglecting intricate interplay mutual modulation observed among various forms PCD. In this comprehensive review, we delineate diverse regulatory governing elucidate crosstalk dynamics distinct pathways. Furthermore, review recent advancements understanding pathogenesis explore their implications DKD. Additionally, potential natural products derived primarily botanical sources therapeutic agents, highlighting multifaceted effects on modulating crosstalk, proposing novel strategies for DKD treatment.

Язык: Английский

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Identification and validation of disulfidptosis-related gene signatures and their subtype in diabetic nephropathy

Frontiers in Genetics, Год журнала: 2023, Номер 14

Опубликована: Ноя. 6, 2023

Background: Diabetic nephropathy (DN) is the most common complication of diabetes, and its pathogenesis complex involving a variety programmed cell death, inflammatory responses, autophagy mechanisms. Disulfidptosis newly discovered mechanism death. There are little studies about role disulfidptosis on DN. Methods: First, we obtained data required for this study from GeneCards database, Nephroseq v5 GEO database. Through differential analysis, disulfidptosis-related genes. At same time, through WGCNA key module genes in DN patients. The intersecting were further screened by Lasso as well SVM-RFE. By results two, ended up with gene diabetic nephropathy. diagnostic performance expression verified GSE30528, GSE30529, GSE96804, datasets. Using clinical information investigated correlation between estimated glomerular filtration rate (eGFR) serum creatinine content. Next, constructed nomogram analyzed immune microenvironment patients identification subtypes facilitates individualized treatment Results: We 91 39 Taking intersection preliminarily 20 characteristic found that these positively correlated each other. Further screening SVM-RFE algorithms identified CXCL6, CD48, C1QB, COL6A3 Clinical analysis levels closely related to eGFR. Immune infiltration higher samples than normal samples. Conclusion: validated 4 may be promote onset eGFR infiltrated kidney tissue.

Язык: Английский

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