Format

Send to

Choose Destination
Inflammation. 2016 Apr;39(2):678-86. doi: 10.1007/s10753-015-0294-y.

Apigenin Attenuates Experimental Autoimmune Myocarditis by Modulating Th1/Th2 Cytokine Balance in Mice.

Author information

1
Biochip Laboratory, Yuhuangding Hospital of Yantai, Affiliated Hospital of Qingdao Medical University, Yantai, 264000, China.
2
Reproductive Medicine Centre, Yuhuangding Hospital of Yantai, Affiliated Hospital of Qingdao Medical University, Yantai, 264000, China.
3
Department of Cardiovascular Disease, Yuhuangding Hospital of Yantai, Affiliated Hospital of Qingdao Medical University, 20 Yuhuangding Road East, Yantai, 264000, China. yangjun151021@163.com.
4
Department of Ultrasound, Yuhuangding Hospital of Yantai, Affiliated Hospital of Qingdao Medical University, Yantai, 264000, China.
5
Department of Cardiovascular Disease, Yuhuangding Hospital of Yantai, Affiliated Hospital of Qingdao Medical University, 20 Yuhuangding Road East, Yantai, 264000, China.

Abstract

This study aims to investigate the protective effect of apigenin on the development of experimental autoimmune myocarditis (EAM) and the underlying mechanisms. An EAM model was induced in BALB/c mice by the injection of porcine cardiac myosin. Apigenin was orally administered from day 1 to 21. The severity of myocarditis was assessed by determination of heart weight/body weight ratio (HW/BW) and histopathological evaluation. Echocardiography was conducted to evaluate the cardiac function and heart structure. Antigen-specific T cell proliferation responses to cardiac myosin were evaluated by the lymphocyte proliferation assay. ELISA was used to determine serum levels of type 1 helper (Th1) and Th2 cytokines. Apigenin treatment significantly decreased HW/BW. Histopathologic analysis showed that the infiltration of inflammatory cells was reduced significantly by apigenin treatment. Meanwhile, apigenin administration effectively ameliorated autoimmune myocarditis-induced cardiac hypertrophy and cardiac dysfunction as well as inhibited lymphocyte proliferation in mice immunized with myosin. Furthermore, Th1 cytokines tumor necrosis factor-alpha (TNF-α), interferon-gamma (IFN-γ), and interleukin-2 (IL-2) were significantly downregulated, while Th2 cytokines IL-4 and IL-10 were markedly upregulated. The results indicated that apigenin can alleviate EAM due to its immunomodulatory reactions in modification of helper T cell balance.

KEYWORDS:

Th1/Th2 cytokine balance; apigenin; experimental autoimmune myocarditis; inflammation; myosin

PMID:
26658748
DOI:
10.1007/s10753-015-0294-y
[Indexed for MEDLINE]

Supplemental Content

Full text links

Icon for Springer
Loading ...
Support Center