Browsing by Subject "Astragaloside IV"

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    Astragaloside IV induces endothelial progenitor cell angiogenesis in deep venous thrombosis through inactivation of PI3K/AKT signaling
    (Universidad de Murcia, Departamento de Biologia Celular e Histiologia, 2024) Lyu, Xiaojiang; Yi, Zhigang; He, Yun; Zhang, Chunfeng; Zhu, Ping; Liu, Chonghai
    Background. Deep vein thrombosis (DVT), referred to as venous thromboembolism, is the third most frequent cardiovascular disease. Endothelial progenitor cells (EPCs) contribute to the recanalization of DVT. Astragaloside IV (AS-IV) has been suggested to have angiogenesis-enhancing effects. Here, we investigate the roles and mechanisms of AS-IV in EPCs and DVT. Methods. The experimental DVT model was established by inferior vena cava stenosis in rats. EPCs were collected from patients with DVT. Transwell assays were performed to detect cell migration. Tube formation was determined using Matrigel basement membrane matrix and ImageJ software. The thrombus weight and length were measured. Pathological changes were examined by hematoxylin-eosin staining. The production of proinflammatory cytokines was estimated by ELISA. The level of PI3K/AKT-related proteins was measured by western blotting. Results. AS-IV administration facilitated the migrative and angiogenic functions of human EPCs in vitro. Additionally, AS-IV inhibited thrombosis and repressed the infiltration of leukocytes into the thrombus and the production of proinflammatory cytokines in rats. Mechanistically, AS-IV inactivated PI3K/AKT signaling in rats. Conclusion. AS-IV prevents thrombus in an experimental DVT model by facilitating EPC angiogenesis and decreasing inflammation through inactivation of PI3K/AKT signaling.
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    Astragaloside IV suppression of chronic atrophic gastritis by upregulating PAR-1 in vitro and in vivo
    (Universidad de Murcia, Departamento de Histología e Histopatología, 2025) Duan Bensong; Bao Zhewei; Yang Jingya; Wang Zhenzhen; Li Aoxiang; Yang Jin; Lv Mengke; Zhang Haibin; Biología Celular e Histología
    Background. Astragaloside IV (AS-IV) has demonstrated a protective effect against gastrointestinal tract injury induced by various factors. However, its potential mechanism against chronic atrophic gastritis (CAG) remains unknown. Purpose. The objective of the present study was to investigate the impact of AS-IV on CAG and elucidate its molecular mechanism. Methods. The mRNA and protein levels of protease-activated receptor-1 (PAR-1) and related proteins were assessed using reverse transcription-polymerase chain reaction and western blot analyses, respectively. In addition, the levels of inflammatory factors were measured via enzyme-linked immunosorbent assay in GES-1 cells following treatment with N-methyl-N'-nitro-N-nitrosoguanidine (MNNG). The CAG model was established in rats induced with MNNG and concurrently treated with AS-IV for 10 weeks. Subsequently, serum samples were collected to assess the expression levels of proteins reflecting inflammatory markers. The gastric tissue sections were used for hematoxylin and eosin staining, immunohistochemical analysis, and the assessment of p-NF-κB p65 and PAR-1 signaling. Results. In-vitro experiments demonstrated that the mRNA levels of PAR-1 were upregulated following treatment with AS-IV and MNNG. Conversely, inhibition of PAR-1 expression reversed the therapeutic effects of AS-IV on MNNG-treated GES-1 cells, leading to increased expression of cyclooxygenase-2 and p-NF-κB p65. In addition, PAR-1 inhibition notably reversed MNNG-induced inflammatory factors, including IL increase. In-vivo experimental validation further confirmed that the upregulation of PAR-1 expression following treatment with AS-IV exerted a protective effect on the gastric mucosa of CAG rats. Conclusion. In conclusion, the findings of the present study suggested that AS-IV exhibited therapeutic efficacy against CAG induced by MNNG; its mechanism may be closely associated with the thrombin/PAR-1 signaling pathway. The present study provides a theoretical foundation for further exploration of the pharmacological effects of AS-IV on the treatment of human CAG