The aim of this study was to investigate whether shear stress could promote function of endothelial progenitor cells (EPCs)with Shexiang Baoxin Pill (SBP) treatment in vitro, and to study whether shear stress contributed to vascular injury repair by EPCs. EPCs were isolated and characterized; EPCs' proliferation, migration, adhesion, tube formation and eNOS protein level in vitro were investigated by culturing confluent EPCs in 4 mg/mL SBP under physiological shear stress (15 dyne/cm2) for up to 24 hours. Afterwards, EPCs were transfused into rats after wire-induced carotid artery injury augmented re-endothelialization. The results showed that, compared to the SBP group, the shear stress+SBP group obviously enhanced EPCs proliferation, migration, adhesion, tube formation and eNOS protein expression in vitro (P<0.01). After one week, immunofluorescence staining showed that endothelial regeneration rate obviously enhanced in shear stress+SBP group (P<0.01). The present study demonstrates that shear stress can promote function of endothelial progenitor cells treated with SBP, which improves the vascular injury repair potentials of EPCs.
Coronary heart disease is a kind of heart disease that is caused by atherosclerosis.The lipid deposition in the vessel wall results in occlusion of coronary artery and stenosis, which could induce myocardial ischemia and oxygen deficiency. Intervention therapies like percutaneous coronary intervention (PCI) and coronary stent improve myocardial perfusion using catheter angioplasty to reduce stenosis and occlusion of coronary artery lumen. Accordingly, intervention therapies are widely applied in clinic to treat ischemic cardiovascular disease, arterial intima hyperplasia and other heart diseases, which could save the patients′ life rapidly and effectively. However, these interventions also damage the original endothelium, promote acute and subacute thrombosis and intimal hyperplasia, and thus induce in stent restenosis (ISR) eventually. Studies indicated that the rapid reendothelialization of damaged section determined postoperative effects. In this review, reendothelialization of implants after intervention therapy is discussed, including the resource of cells contributed on injured artery, the influences of implanted stents on hemodynamic, and the effects of damaged degree on reendothelialization.
Cardiovascular disease is one of the most common causes of death. Coronary artery stent implantation has been the most important method to cure coronary disease and inhibit angiostegnosis. However, restenosis and thrombus at the site of implanting cardiovascular devices remains a significant problem in the practice of interventional cardiology. Recently, lots of studies have revealed that endothelial impairment is considered as one of the most important mechanisms contributing to restenosis. As a result, the method of accelerating endothelial regeneration at the injury site could prevent restenosis and thrombus. Considering the surface modification of cardiovascular stent implantation, this paper summarizes the progress on this direction, especially for the prevention of cardiovascular restenosis. Furthermore, this paper also proposes the methods and the future developing prospects for accelerating in vivo re-endothelialization at the site of intravascular stent with different biological molecules.
The presence of thrombus on the surface of blood-contacting biomaterials in clinical practice can significantly impact both the longevity of the biomaterials and the overall survival prognosis of patients. The administration of anticoagulant and antiplatelet medications may heighten the risk of systemic bleeding. Developing biomaterials with anti-thrombogenetic properties and enabling localized anti-thrombosis may offer a solution to these challenges. The development strategies for anti-thrombogenetic biomaterials can be categorized into three main approaches based on the mechanisms of thrombus formation on biomaterial surfaces: altering physical and chemical properties, designing coatings containing or releasing active substances, and promoting endothelialization. However, due to the intricate and interconnected nature of these mechanisms, biomaterials constructed using a single approach may not effectively prevent thrombus formation. The collaborative intervention of various mechanisms can facilitate the development of biomaterials with enhanced blood compatibility.