<i>Pinellia ternata</i> attenuates carotid artery intimal hyperplasia and increases endothelial progenitor cell activity via the PI3K/Akt signalling pathway in wire-injured rats

Clinically, <i>Pinellia ternata</i> (Thunb.) Breit. (Araceae) (<i>PT</i>) has been widely used in the treatment of atherosclerosis and hyperlipidaemia, but the underlying mechanisms are still not clearly understood. This research was conducted to confirm the mechanism by which <i>PT</i> affects carotid artery intimal hyperplasia. An intestinal hyperplasia Sprague-Dawley rat model was established by carotid artery injury. The rats were randomly divided into five groups (<i>n</i> = 8): sham, model, <i>PT</i> (with daily intragastric administration of 10 g/mL/kg <i>PT</i> tubers water extract), <i>PT</i>+LY294002 (with intraperitoneal injection of 50 mg/kg LY294002 + 10 g/mL/kg <i>PT</i>) and endothelial progenitor cells (EPCs) (with injection of 5 × 10⁵/cells), and treated for 4 or 8 weeks. HE staining showed that <i>PT</i> attenuated intimal hyperplasia. RT-PCR, Western blotting and immunohistochemistry showed that <i>PT</i> increased the expression of vascular endothelial growth factor (VEGF) and eNOS in the atherosclerotic carotid artery. <i>PT</i> 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. <i>PT</i> can be developed as an atherosclerosis and carotid intimal hyperplasia treatment drug. Therefore, further study will focus on the effects of <i>PT</i> on intimal hyperplasia in wire-injured atherosclerosis patients and explore in depth some other relevant molecular mechanisms.