People exposed to radiation in cancer therapy and nuclear accidents are at increased risk of cardiovascular outcomes in long‐term survivors. Extracellular vesicles (EVs) are involved in radiation‐induced endothelial dysfunction, but their role in the early stage of vascular inflammation after radiation exposure remains to be fully understood. Herein, we demonstrate that endothelial cell‐derived EVs containing miRNAs initiate monocyte activation in radiation‐induced vascular inflammation. In vitro co‐culture and in vivo experimental data showed that endothelial EVs can be sensitively increased by radiation exposure in a dose‐dependent manner, and stimulate monocytes releasing monocytic EVs and adhesion to endothelial cells together with an increase in the expression of genes encoding specific ligands for cell‐cell interaction. Small RNA sequencing and transfection using mimics and inhibitors explained that miR‐126‐5p and miR‐212‐3p enriched in endothelial EVs initiate vascular inflammation by monocyte activation after radiation exposure. Moreover, miR‐126‐5p could be detected in the circulating endothelial EVs of radiation‐induced atherosclerosis model mice, which was found to be tightly correlated with the atherogenic index of plasma. In summary, our study showed that miR‐126‐5p and miR‐212‐3p present in the endothelial EVs mediate the inflammatory signals to activate monocytes in radiation‐induced vascular injury. A better understanding of the circulating endothelial EVs content can promote their use as diagnostic and prognostic biomarkers for atherosclerosis after radiation exposure.

Pseudostellaria heterophylla (PH) has various pharmacological effects that include immunologic enhancement and anti‑oxidation. However, it remains unclear whether PH exerts beneficial effects in dermatological diseases. The present study examined the effects of PH on a 2,4-dinitrochlorobenzene (DNCB)‑induced atopic dermatitis (AD) mouse model and elucidated its underlying mechanism of action. PH extract (1 and 100 mg/ml) was applied topically to DNCB-treated dorsal skin of mice every day for 11 days. The immunomodulatory effects of PH were evaluated by measuring skin thickness, mast cell infiltration, serum levels of immunoglobulin E (IgE), and mRNA expression levels of T helper (h)1/Th2 and pro‑inflammatory cytokines in dorsal skin. In addition, cluster of differentiation (CD)4+ T cells were detected in dorsal skin by immunohistochemistry. Topical application of PH significantly reduced the thickness of dermis, epidermis and serum IgE production compared with the DNCB group. PH treatment inhibited infiltration of inflammatory cells, including mast cells and CD4+ T cells, and suppressed the mRNA expression levels of cytokines (interferon‑γ, interleukin‑4, ‑6, ‑8 and ‑1β, and tumor necrosis factor‑α) associated with the immune response. Furthermore, PH treatment significantly downregulated the protein expression levels of nuclear factor‑κB, phosphorylated inhibitor of κBα and mitogen‑activated protein kinases. The results suggested that PH may be a potential therapeutic strategy for the treatment of AD via the modulation of Th1 and Th2 levels.