Investigating the Effect and Mechanism of 3-Methyladenine Against Diabetic Encephalopathy by Network Pharmacology, Molecular Docking, and Experimental Validation DOI Creative Commons

Jiaxin Chu,

Jianqiang Song,

Zhonghang Fan

и другие.

Pharmaceuticals, Год журнала: 2025, Номер 18(5), С. 605 - 605

Опубликована: Апрель 22, 2025

Background/Objectives: Diabetic encephalopathy (DE), a severe neurological complication of diabetes mellitus (DM), is characterized by cognitive dysfunction. 3-Methyladenine (3-MA), methylated adenine derivative, acts as biomarker for DNA methylation and exhibits hypoglycemic neuroprotective properties. However, the pharmacological mechanisms underlying 3-MA’s therapeutic effects on diabetic microvascular complications remain incompletely understood, owing to intricate multifactorial pathogenesis DE. Methods: This study employed network pharmacology molecular docking techniques predict potential targets signaling pathways 3-MA against DE, with subsequent validation through animal experiments elucidate in DE treatment. Results: Network analysis identified two key modulation: AKT GSK3β. Molecular confirmed strong binding affinity between AKT/GSK3β. In experiments, significantly reduced blood glucose levels mice, ameliorated learning memory deficits, preserved hippocampal neuronal integrity. Furthermore, we found that inhibited apoptosis regulating expression Bax BCL-2. Notably, also downregulated amyloid precursor protein (APP) Tau while enhancing phosphorylated GSK-3β. Conclusions: Our findings may contribute elucidating microangiopathy provide activation AKT/GSK-3β pathway.

Язык: Английский

Kurarinone Attenuates LPS‐Induced Pneumonia by Inhibiting MAPK and NF‐κB Signaling Pathways DOI
Lili Wang,

Guoyu Lu,

Fangli Wang

и другие.

Apmis, Год журнала: 2025, Номер 133(3)

Опубликована: Март 1, 2025

Kurarinone is a prenylated flavanone isolated from Sophora flavescens Aiton. This investigation aimed to elucidate whether kurarinone could ameliorate lipopolysaccharide (LPS)-induced pneumonia and explore the underlying mechanism. C57BL/6 mice were treated with LPS (50 μg/20 μL) establish models. (100 mg/kg) or dexamethasone (DEX, 5 was administered for 7 days before inhalation. BEAS-2B cells incubated at 1, 2, μM 2 h stimulation 24 h. We found that ameliorated lung injury inflammatory cell infiltration in mouse (p < 0.001). decreased MPO activity (47.6%, p 0.001) alleviated response by reducing levels of IL-1β (34.9%, 0.001), TNF-α (55.1%, IL-6 (36.2%, lung. reduced IL-1β, TNF-α, IL-6, iNOS, COX2 LPS-treated concentration-dependent manner 0.05). Mechanistically, restrained LPS-induced activation MAPK NF-κB pathways vivo vitro Overall, alleviates inflammation via pathways, suggesting might be potential therapeutic agent pneumonia. study provides new research ideas discovery natural flavonoids can treat

Язык: Английский

Процитировано

0
Thesium Chinense Turcz. and Its Compound Astragalin Alleviate Lipopolysaccharide-Induced Acute Lung Injury via the PI3K/AKT/p53 Signaling Pathway DOI
Haonan Xu,

Fang Zhang,

Che Yan

и другие.

Journal of Ethnopharmacology, Год журнала: 2025, Номер unknown, С. 119691 - 119691

Опубликована: Март 1, 2025

Язык: Английский

Процитировано

0
Investigating the Effect and Mechanism of 3-Methyladenine Against Diabetic Encephalopathy by Network Pharmacology, Molecular Docking, and Experimental Validation DOI Creative Commons

Jiaxin Chu,

Jianqiang Song,

Zhonghang Fan

и другие.

Pharmaceuticals, Год журнала: 2025, Номер 18(5), С. 605 - 605

Опубликована: Апрель 22, 2025

Background/Objectives: Diabetic encephalopathy (DE), a severe neurological complication of diabetes mellitus (DM), is characterized by cognitive dysfunction. 3-Methyladenine (3-MA), methylated adenine derivative, acts as biomarker for DNA methylation and exhibits hypoglycemic neuroprotective properties. However, the pharmacological mechanisms underlying 3-MA’s therapeutic effects on diabetic microvascular complications remain incompletely understood, owing to intricate multifactorial pathogenesis DE. Methods: This study employed network pharmacology molecular docking techniques predict potential targets signaling pathways 3-MA against DE, with subsequent validation through animal experiments elucidate in DE treatment. Results: Network analysis identified two key modulation: AKT GSK3β. Molecular confirmed strong binding affinity between AKT/GSK3β. In experiments, significantly reduced blood glucose levels mice, ameliorated learning memory deficits, preserved hippocampal neuronal integrity. Furthermore, we found that inhibited apoptosis regulating expression Bax BCL-2. Notably, also downregulated amyloid precursor protein (APP) Tau while enhancing phosphorylated GSK-3β. Conclusions: Our findings may contribute elucidating microangiopathy provide activation AKT/GSK-3β pathway.

Язык: Английский

Процитировано

0