Astragaloside IV targeting autophagy of T cells improves inflammation of asthma

Abstract

Astragaloside IV (AST) has been confirmed to have antiasthmatic effects. However, the underline mechanism is unclear. The study aimed to explore the treatment mechanism of AST based on autophagy of memory T cells. AST treatment significantly decreased the number of T effector cells in asthma mice blood and the nude mice that received AST-treated T_CMs had relieved inflammation compared with the untreated group; meanwhile, we found that AST significantly decreased the autophagy level and inhibited OX40/OX40L signal pathway of lymphocytes. The results highlighted that AST regulated autophagy to inhibit differentiation of effector T-cell phenotype.

Keywords:

• Asthma recurrence
• CC chemokine receptor (CCR) 7
• memory T cells
• astragaloside IV
• autophagy

Acknowledgements

Not applicable.

Authors’ contributions

Conceptualization: Lingwen Kong and Xiaohong Duan; Methodology: Lingwen Kong, Qingqing Yang and Hongying Zhang; Formal analysis and investigation: Lingwen Kong; Writing-original draft preparation: Lingwen Kong and Chen Yan; Writing-review and editing: Lingwen Kong, Jingcheng Dong and Mihui Li; Funding acquisition: Lingwen Kong and Jing Sun; Resources: Lingwen Kong and Xiaohong Duan; Supervision: Lingwen Kong and Jingcheng Dong.

Ethics approval and consent to participate

All animal experiments were performed following the Guide for the Care and Use of Laboratory Animals, and all animal experimental procedures used in this study were approved by the Fudan University of Animal Ethics Committee. All surgery was performed under sodium pentobarbital anesthesia, and all efforts were made to minimize suffering.

Consent for publication

Not applicable.

Disclosure statement

We wish to confirm that there are no known conflicts of interest associated with this publication and there has been no significant financial support for this work that could have influenced its outcome.

Availability of data and materials

The datasets used and/or analyzed during the current study are available from the corresponding author on reasonable request.

Additional information

Funding

This work was financially supported by the National Natural Science Foundation of China (Grant No. 81503483/H2704) and Shanghai science and technology commission scientific research project (Grant 18401901800).