Dihydroartemisinin ameliorates balloon injury‐induced neointimal formation in rats

Abstract

Objectives This study aims to evaluate the effects of dihydroartemisinin (DHA) on the balloon injury‐induced neointimal formation in rats and to investigate the underlying mechanism. Methods The balloon‐induced carotid artery injury model was established in male Sprague–Dawley rats, immediately after which the DHA solution was injected into the tail vein of rats. In in vitro assays, primary rat vascular smooth muscle cells (VSMCs) were pretreated with DHA and then coincubated with LPS. Results DHA ameliorated the induced neointimal formation and fibrosis but enhanced apoptosis in rat carotid artery after balloon injury. Furthermore, DHA suppressed migration and enhanced apoptosis of the lipopolysaccharide (LPS)‐treated primary VSMCs in vitro. Moreover, in both the balloon injury‐induced rat sera and the LPS‐treated VSMCs, DHA significantly inhibited proinflammatory cytokines, including interleukin‐1β, tumor necrosis factor‐ɑ, and matrix metalloproteinase‐1. Importantly, DHA significantly decreased the balloon injury‐increased expression of nuclear factor kappa B (NF‐κB) subunit NF‐κB p65 expression, and increased the balloon injury‐reduced expression of inhibitor of NF‐κB‐alpha, indicating the inhibition of the IκB/NF‐κB pathway. Conclusion DHA significantly inhibited neointimal formation in balloon‐induced rat carotid artery injury and the mechanism may be related to the inhibition of IκB/NF‐κB signaling, which alleviates the inflammatory response.

Exosomes of endothelial progenitor cells repair injured vascular endothelial cells through the Bcl2/Bax/Caspase-3 pathway

“…This remarkable therapeutic outcome underscores the potential of exosome-based treatment as a novel and promising cell-free vascular repair therapeutic option. According to recent pharmacological research, the primary mechanisms underlying the recurrence of vascular stenosis post-PCI involve the proliferation and migration of smooth muscle cells (SMCs) close to the endothelial injury site 29 . Hence, most medications employed to mitigate restenosis are aimed at inhibiting SMC proliferation.…”