ArticleJournal of molecular histology2025
Coptisine alleviates high glucose-induced HUVEC dysfunction in vitro and inhibits gestational diabetes mellitus in vivo.
Article in Journal of molecular histology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
1 citing paper in PubMed.
- Current status and research trends of coptisine: a bibliometric analysis (1995 to 2025).Naunyn-Schmiedeberg's archives of pharmacology · 2026Review
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Authors and funding
3 authors.
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Abstract
The dysfunction of vascular endothelial cells (VECs) is an important cause of diabetes-related cardiovascular diseases. Coptisine is a bioactive component of Rhizoma coptidis with anti-diabetes property. The aim of this present study was to clarify the role and possible mechanism of coptisine underlying VEC dysfunction during gestational diabetes mellitus (GDM). Human umbilical vein endothelial cells (HUVECs) were treated with coptisine and/or high glucose (HG) medium. A GDM rat model was established by high-fat diet feeding and streptozotocin injection. Cell viability, migration, and angiogenesis were detected by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay, wound healing assay, Transwell assay, and tube formation assay. The levels of angiogenesis-related proteins and the key markers in the Adenosine monophosphateactivated protein kinase (AMPK)/nuclear factor-erythroid 2-related factor 2 (NRF2) signaling pathway were tested by western blot analysis. The pathological changes of placental tissues were observed by HE staining. We found that the cell viability of HUVECs was repressed in HG conditions in a dose-dependent manner, and 25 mM HG reduced the HUVEC viability in a time-dependent manner. Coptisine (5 to 5o μM) did not cause cytotoxicity to HUVECs. In addition, HG-induced the decrease in cell viability and migration of HUVECs were rescued by coptisine in a dose-dependent manner. Coptisine restored the angiogenetic ability of HG-induced HUVECs by upregulating the protein expression of fibroblast growth factor 2, vascular endothelial-derived growth factor, and Angiotensin 1. Moreover, coptisine treatment re-activated the AMPK/NRF2 pathway in HG-stimulated HUVECs. Importantly, inhibition of AMPK/NRF2 signaling reverses the effect of coptisine on cell viability, migration, and angiogenesis of HUVECs. The in vivo study demonstrated that coptisine suppresses hyperglycemia and placenta injury in GDM rats. Coptisine protected HUVECs from hyperglycemic insult, suggesting the potential of coptisine which might be used as a therapeutic agent for VEC dysfunction in GDM.
Indexed as
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40781493What Socratic holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.