ArticleMolecular medicine reports2017
The effect of anagliptin on intimal hyperplasia of rat carotid artery after balloon injury.
Article in Molecular medicine reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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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
3 citing papers in PubMed, 7 citations in OpenAlex.
- Molecular Action of Hydroxytyrosol in Attenuation of Intimal Hyperplasia: A Scoping Review.Frontiers in pharmacology · 2021Article
- Platelet-Derived Microvesicles Promote VSMC Dedifferentiation After Intimal Injury via Src/Lamtor1/mTORC1 Signaling.Frontiers in cell and developmental biology · 2021Article
- Linagliptin protects rat carotid artery from balloon injury and activates the NRF2 antioxidant pathway.Experimental animals · 2019Article
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The present study evaluated the effect of anagliptin on intimal hyperplasia following carotid artery injury in Sprague‑Dawley rats. Sprague‑Dawley rats weighing 280‑300 g were injured using a 2F Fogarty balloon embolectomy catheter. The rats were divided into injury‑(saline) and anagliptin‑(10 mg/kg/day) treated groups. vascular injuries were induced in the left carotid artery, followed by evaluation of neointima formation at 28 days. The right and left carotid arteries were harvested and evaluated with histological evaluation, and the plasma activity of glucagon‑like peptide 1 receptor (GLP‑1), stromal cell‑derived factor (SDF)‑1α, interleukin (IL)‑6, IL‑1β and tumor necrosis factor (TNF)‑α were detected by ELISA analysis. Treatment with anagliptin decreased balloon injury‑induced neointima formation, compared with the injury group (P<0.01). Body weight and food consumption did not alter following treatment with anagliptin. Anagliptin caused an increase in the serum active GLP‑1 concentration, compared with the injury group. In addition, serum SDF‑1α was significantly decreased by treatment with anagliptin (P<0.001). Anagliptin altered the serum activity of IL‑6, IL‑1β and TNF‑α (P<0.01). The results of the present study demonstrated that anagliptin appeared to attenuate neointimal formation by inhibiting inflammatory cytokines and chemokines following balloon injury, and that treatment with a dipeptidyl peptidase 4 inhibitor may be useful for future preclinical studies and potentially for the inhibition of thrombosis formation following percutaneous coronary intervention.
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