Abstract

Urticaria symptoms and disease severity exhibit a 24 h cycle, with circadian rhythms influencing skin tissue apoptosis. This study sought to evaluate the impact of astragaloside IV on core circadian gene expression and cell apoptosis in mice with urticaria-like lesions. Sixty mice were allocated to three groups at random, including a normal group (administered with saline), a model group (administered with ovalbumin and aluminum), and an astragaloside IV group (50 mg/kg/d). Each group was further subdivided into zeitgeber time 0 and zeitgeber time 12 subgroups. Allergic reactions, behavioral rhythms and histopathology were assessed in urticaria-like mice. Serum concentrations of immunoglobulin E, histamine and leukotriene B4 were determined by enzyme-linked immunosorbent assay; cell apoptosis was assessed by terminal deoxynucleotidyl transferase dUTP nick end labeling technique; the levels of protein of p53 and B-cell lymphoma 2 were analyzed by Western blot and immunohistochemistry, and reverse transcription quantitative-polymerase chain reaction was applied to determine messenger ribonucleic acid levels of brain and muscle ARNT-like, circadian locomotor output cycles kaput, period 2, and cryptochrome 1. The findings demonstrated that astragaloside IV significantly reduced allergic and inflammatory responses in urticaria-like mice and lowered serum inflammatory factors. Astragaloside IV also enhanced apoptosis in skin tissues by increasing p53 and decreasing B-cell lymphoma 2 levels. Furthermore, astragaloside IV elevated messenger ribonucleic acid levels of BMAL1, circadian locomotor output cycles kaput, and period 2, while reducing cryptochrome 1 expression in the suprachiasmatic nuclei. Mice showed a greater therapeutic response to astragaloside IV at zeitgeber time 12. In conclusion, astragaloside IV facilitates apoptosis and regulates circadian rhythm gene expression in urticaria-like mice, with its effects being dependent on the timing of administration.