AI Article Synopsis

  • The study aimed to investigate the impact of Astragalus membranaceus (AM) on the expression of Th17 cells and related factors in patients with allergic rhinitis (AR).
  • It involved sampling blood cells from 31 AR patients and 22 healthy controls, followed by treating these cells with two different doses of AM in a lab setting.
  • Results showed that high-dose AM significantly reduced the levels of Th17 and related cytokines in both groups, suggesting that AM may help control inflammation in allergic rhinitis by inhibiting Th17 cell differentiation.

Article Abstract

Objective To observe the effect of Astragalus membranaceus (AM) on expression levels of helper T cell 17 (Th17) and its related factors in patients with allergic rhinitis (AR). Methods Peripheral blood mononuclear cells (PBMCs) were sampled from 31 AR patients (recruited in the AR group) and 22 healthy subjects (recruited in the control group). PBMCs were isolated and in-vitro inter- vened by high and low dose AM injection (2 000 and 500 μg/mL) respectively for 24 h. mRNA expression levels of related orphan receptor C (RORC) were detected by real time quantitative PCR (RT-qPCR). Ex- pression levels of IL-17A and IL-22 in the supernatant were measured by ELISA. Expression levels of Th17 cells were measured by flow cytometry. Results Expression levels of Th17, RORC mRNA, IL- 17A, and IL-22 were higher in the AR group than in the control group (P <0. 01). mRNA expression levels of RORC, Th17 and its cytokines were not changed statistically in the AR group and the control group after PBMCs were intervened by low dose AM (P>0. 05). After intervened by high dose AM,mRNA expres- sion levels of RORC decreased statistically in the AR group and the control group (P <0. 05 for the AR group, P <0. 01 for the control group). Meanwhile,the expression levels of Th-17 and its cytokines de- creased in the AR group and the control group with statistical difference (P <0. 01). Conclusions Ex- cessive activation of Th17 is one of key factors-for AR. AM could further inhibit inflammation of AR and control the inflammation state of AR possibly through inhibiting the differentiation of Th17 cells and promo- ting the release of its cytokines.

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