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Attenuates Carotid Artery Intimal Hyperplasia and Increases Endothelial Progenitor Cell Activity Via the PI3K/Akt Signalling Pathway in Wire-injured Rats

Overview
Journal Pharm Biol
Specialties Pharmacology
Pharmacy
Date 2020 Nov 30
PMID 33253601
Citations 3
Authors
Affiliations
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Abstract

Context: Clinically, (Thunb.) Breit. (Araceae) () has been widely used in the treatment of atherosclerosis and hyperlipidaemia, but the underlying mechanisms are still not clearly understood.

Objective: This research was conducted to confirm the mechanism by which affects carotid artery intimal hyperplasia.

Materials And Methods: An intestinal hyperplasia Sprague-Dawley rat model was established by carotid artery injury. The rats were randomly divided into five groups ( = 8): sham, model, (with daily intragastric administration of 10 g/mL/kg tubers water extract), +LY294002 (with intraperitoneal injection of 50 mg/kg LY294002 + 10 g/mL/kg ) and endothelial progenitor cells (EPCs) (with injection of 5 × 10/cells), and treated for 4 or 8 weeks.

Results: HE staining showed that attenuated intimal hyperplasia. RT-PCR, Western blotting and immunohistochemistry showed that increased the expression of vascular endothelial growth factor (VEGF) and eNOS in the atherosclerotic carotid artery. increased the Dil-acLDL/FITC-UEA-1 population (from 0.41 ± 0.085% to 0.60 ± 0.092%) in the blood, decreased TCHO, TG, LDL-C, IL-6 and TNF-α levels, and increased HDL-C and IL-10 levels in the blood. However, these changes were reversed by the PI3K/Akt pathway inhibitor LY294002.

Discussion And Conclusions: can be developed as an atherosclerosis and carotid intimal hyperplasia treatment drug. Therefore, further study will focus on the effects of on intimal hyperplasia in wire-injured atherosclerosis patients and explore in depth some other relevant molecular mechanisms.

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