The effect of anagliptin on intimal hyperplasia of rat carotid artery after balloon injury

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.

Linagliptin protects rat carotid artery from balloon injury and activates the NRF2 antioxidant pathway

“…In addition, a report from Li et al. showed that anagliptin, the DPP-4 inhibitor, attenuated neointima formation in rats suffered balloon injury by preventing the production of inflammatory cytokines and chemokines [18]. In agreement with these studies, we found that the levels of TNF-α, IL-1β and IL-6 in the cervical aorta of rats were increased after balloon injury, and linagliptin inhibited the production of these inflammatory factors dose dependently.…”

DPP-4 inhibitor anagliptin protects against hypoxia-induced cytotoxicity in cardiac H9C2 cells

“…In a murine atherosclerosis model, the treatment of mice with anagliptin reduced aortic plaque burden [9]. In induced vascular injury rats, administration of anagliptin reduces neointimal formation and relieves whole-body inflammation [10]. In a vascular aneurysm model, the treatment of animals by anagliptin significantly reduces the size of intracranial aneurysms and suppresses inflammatory pathway in macrophages [11].…”

Platelet-Derived Microvesicles Promote VSMC Dedifferentiation After Intimal Injury via Src/Lamtor1/mTORC1 Signaling

“…In normal adult, VSMCs maintains a contractile phenotype which proliferates slowly and expresses a range of contractile proteins for functional contraction. In response to vascular injury or local environmental alteration, contractile VSMCs dedifferentiate to synthetic phenotype ( Allahverdian et al, 2018 ), characterized as repressed contractile proteins, altered morphology from elongated/spindle-like to thomboid/epitheloid-like, increased proliferation, and facilitated migration ( Li et al, 2017 ). In healthy vascular wall, individual VSMC dedifferentiation occurs at a low event rate which participates in vascular wall repair.…”