Scutellarin ameliorates ischemia/reperfusion-mediated endothelial dysfunction by upregulating cathepsin D expression to rescue autophagy-lysosomal function DOI Creative Commons
Qi-Zhen Zhuang, Lu Chen, V. Wu

и другие.

Frontiers in Pharmacology, Год журнала: 2025, Номер 16

Опубликована: Март 3, 2025

Background Endothelial dysfunction-induced microcirculation impairment and the no-reflow phenomenon are leading causes of cardiac ischemia/reperfusion (I/R) injury. There is an urgent need to elucidate underlying mechanism I/R-mediated endothelial dysfunction identify effective drugs for treatment. Scutellarin (SCU), a flavonoid compound, has been extensively studied because its various pharmacological properties, including potent protective effects on cardiovascular system. However, anti-endothelial efficacy mechanisms action SCU have not investigated. Approach results An in vivo I/R injury model was established using coronary artery ligation release. oxygen-glucose deprivation/oxygen-glucose resupply (OGD/OGR) approach used establish vitro model. We evaluated under conditions, both . pretreatment promoted vasodilation reperfusion blood flow, inhibited myocardial infarction, improved function rats. Additionally, cell membrane damage, reactive oxygen species (ROS) accumulation, inflammation, nitric oxide (NO) reduction, endothelin 1 (ET-1) elevation increase expression levels vascular growth factor (VEGF) von willebrand (vWF) cells. Mechanistically, rescued lysosomal flow autophagic flux disrupted by through upregulating cathepsin D (CTSD) levels. Knockdown CTSD or treatment with inhibitor pepstatin A (P.A) abrogated cells conditions. Conclusion demonstrated that SCU, via upregulation cells, autophagy-lysosomal alleviated dysfunction. Thus, potential therapeutic drug prevention

Язык: Английский

Current Advances in the Therapeutic Potential of Scutellarin: Novel Applications, Mechanisms, and Future Challenges. DOI Creative Commons
Great Iruoghene Edo, Alice Njolke Mafe, Patrick Othuke Akpoghelie

и другие.

Phytomedicine Plus, Год журнала: 2025, Номер unknown, С. 100754 - 100754

Опубликована: Янв. 1, 2025

Язык: Английский

Процитировано

2

Exploring the Mechanism of Wu-Mei-Wan in Treating Metabolic Syndrome Through Liver Autophagy Pathway Based on Bioinformatics and Omics Analysis DOI
Ming Guo, Xuelin Zhou, Haodong Zhang

и другие.

Опубликована: Янв. 1, 2025

Ethnopharmacological relevance:Metabolic syndrome (MetS) is a pathological condition characterized by obesity, hyperglycemia, hypertension, and hyperlipidemia, which increases the risk of cardiovascular disease, type 2 diabetes, non-alcoholic fatty liver disease. The traditional Chinese medicine Wu-Mei-Wan (WMW) formula, modified from Shanghanlun, has long been used in clinical practice for gastrointestinal metabolic disorders. However, pharmacological mechanisms WMW treatment MetS remain unclear.Aim study: Here, we explored actions on via network pharmacology validated mechanism mice.Materials methods: A involving intersecting genes active components was delineated. top proteins underwent molecular docking. And findings were using RT-PCR. high fat diet induced mice model treated with WMW, indicators ELISA, HE staining, oil red staining. Metabolome analysis conducted both serum feces mice, while 16S microbiota sequencing specifically performed their feces. Ultimately, comprehensive omics carried out, integrating insights metabolomic analyses.Results: study revealed that improved blood biochemical function played significant role protection. Network demonstrated compounds have therapeutic effects modulating lipids, atherosclerosis. Furthermore, increased expression levels PINK1 suggested autophagy exerts protective effect syndrome. Metabolomic disruptions pathways involved lipid metabolism. Joint indicated strong correlation between these factors.Conclusion: In this can enhance pathway activity thereby alleviating protected against injury through oxidative stress, offering new into its potential.

Язык: Английский

Процитировано

0

Scutellarin ameliorates ischemia/reperfusion-mediated endothelial dysfunction by upregulating cathepsin D expression to rescue autophagy-lysosomal function DOI Creative Commons
Qi-Zhen Zhuang, Lu Chen, V. Wu

и другие.

Frontiers in Pharmacology, Год журнала: 2025, Номер 16

Опубликована: Март 3, 2025

Background Endothelial dysfunction-induced microcirculation impairment and the no-reflow phenomenon are leading causes of cardiac ischemia/reperfusion (I/R) injury. There is an urgent need to elucidate underlying mechanism I/R-mediated endothelial dysfunction identify effective drugs for treatment. Scutellarin (SCU), a flavonoid compound, has been extensively studied because its various pharmacological properties, including potent protective effects on cardiovascular system. However, anti-endothelial efficacy mechanisms action SCU have not investigated. Approach results An in vivo I/R injury model was established using coronary artery ligation release. oxygen-glucose deprivation/oxygen-glucose resupply (OGD/OGR) approach used establish vitro model. We evaluated under conditions, both . pretreatment promoted vasodilation reperfusion blood flow, inhibited myocardial infarction, improved function rats. Additionally, cell membrane damage, reactive oxygen species (ROS) accumulation, inflammation, nitric oxide (NO) reduction, endothelin 1 (ET-1) elevation increase expression levels vascular growth factor (VEGF) von willebrand (vWF) cells. Mechanistically, rescued lysosomal flow autophagic flux disrupted by through upregulating cathepsin D (CTSD) levels. Knockdown CTSD or treatment with inhibitor pepstatin A (P.A) abrogated cells conditions. Conclusion demonstrated that SCU, via upregulation cells, autophagy-lysosomal alleviated dysfunction. Thus, potential therapeutic drug prevention

Язык: Английский

Процитировано

0