Ferroptosis inhibitor regulates the disease progression of systematic lupus erythematosus mice model through Th1/Th2 ratio

Author:

Yang Bo1,Hou Shihao2,Huang Shiqing2,Li Hongwen1,Li Yepeng2

Affiliation:

1. Key Laboratory of Guangxi College and Universities, Biomedical Research Center, The Affiliated Hospital of Youjiang Medical University for Nationalities, Baise 533000, Guangxi, China

2. Department of Oncology, The Affiliated Hospital of Youjiang Medical University for Nationalities, Baise 533000, Guangxi, China

Abstract

Background: Systematic lupus erythematosus (SLE) is an autoimmune-mediated disease. So far, there is no relevant report on ferroptosis in SLE research, and the role of T helper 1 (Th1) and T helper 2 (Th2) cells in SLE is still unclear. Methods: This study employed SLE mice models with and without ferroptosis inhibitors(Liproxstatin‑1) and normal control mice. Treated mice were zanalyzed with hematoxylin and eosin (H&E) staining, immunohistochemical detection of glutathione peroxidase 4 (GPX4), malondialdehyde (MDA) detection, ELISA(enzyme-linked immunosorbent assay) detection of Th1 and Th2 cytokines and flow cytometry detection of Th1 and Th2 ratio. Results: The results showed that compared with the normal group, the SLE group exhibited significantly higher expression of anti-double-stranded deoxyribonucleic acid (anti-dsDNA), MDA and Th1 cytokines, significantly lower expression of GPX4 and Th2 cytokines and increased Th1/Th2 ratio. Similarly, compared with the SLE group, the SLE + liproxstatin-1 group showed significantly low expression of anti-dsDNA, MDA and Th1 cytokines, significantly high expression of GPX4 and Th2 cytokines and reduced Th1/Th2 ratio. Conclusion: These results demonstrate that ferroptosis may be involved in promoting SLE development. Therefore, inhibiting ferroptosis may be a potential treatment for SLE. Similarly, the Th1/Th2 ratio may have a role in promoting SLE development.

Publisher

Bentham Science Publishers Ltd.

Subject

Molecular Biology,Molecular Medicine,General Medicine,Biochemistry

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