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Am J Physiol Renal Physiol. 2016 Jul 1;311(1):F217-26. doi: 10.1152/ajprenal.00249.2015. Epub 2016 Feb 24.

Quercitrin ameliorates the development of systemic lupus erythematosus-like disease in a chronic graft-versus-host murine model.

Author information

1
Beijing Key Laboratory of Gene Engineering and Biotechnology, Department of Biochemistry and Molecular Biology, Beijing Normal University, Beijing, China;
2
College of Pharmacy, Hubei University of Chinese Medicine, Wuhan, China; and.
3
Department of Pathology, University of Florida, Gainesville, Florida.
4
Beijing Key Laboratory of Gene Engineering and Biotechnology, Department of Biochemistry and Molecular Biology, Beijing Normal University, Beijing, China; weiq@bnu.edu.cn.

Abstract

Systemic lupus erythematosus (SLE) is a serious disorder of immune regulation characterized by overproduction of autoantibodies, lupus nephritis, CD4+ T cell aberrant activation, and immune complex-mediated inflammation. The chronic graft vs. host disease (cGVHD) mouse model is a well-established model of SLE. Quercitrin is a natural compound found in Tartary buckwheat with a potential anti-inflammatory effect that is used to treat heart and vascular conditions. In our previous study, we determined that quercitrin is an immunosuppressant with beneficial effects in mouse models of immune diseases. We hypothesized that quercitrin could prevent lupus nephritis in the cGVHD mouse model by decreasing the production of autoantibodies and inflammatory cytokines, and reducing immune cell activation. cGVHD was induced by injecting DBA/2 spleen cells into the tail vein of BDF1 mice. The cGVHD mice exhibited significant proteinuria, which is a marker of nephritis. Quercitrin decreased the number of serum antibodies, CD4+ T cell activation, as well as the expression levels of T-bet, GATA-3, and selected cytokines. Moreover, quercitrin treatment decreased the expression of inflammatory genes and cytokines in the kidney, as well as in peritoneal macrophages. In addition, quercitrin inhibited LPS-induced cytokines as well as the phosphorylation of ERK, p38 MAPK, and JNK in Raw264.7 cells. Overall, quercitrin ameliorated the symptoms of lupus nephritis in the cGVHD mouse model, which may be due to the inhibition of CD4 T cell activation and anti-inflammatory effects on macrophages.

KEYWORDS:

CD4+ T cells; chronic graft versus host disease; inflammation; quercitrin; systemic lupus erythematosus

PMID:
26911849
DOI:
10.1152/ajprenal.00249.2015
[Indexed for MEDLINE]
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