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Study on the anti‐atherosclerotic mechanisms of immune tolerance induced by heat shock protein 60
Author(s) -
Hao Chunyan,
Duan Hubin,
Li Shuzhen,
Wang Suping,
Xiao Chuanshi,
Liu Xuejun,
Xi Ling,
Wang Fengzhi
Publication year - 2013
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.27.1_supplement.551.2
Subject(s) - hsp60 , heat shock protein , cd36 , immune system , flow cytometry , immunohistochemistry , medicine , western blot , immunology , pathology , hsp70 , biology , receptor , gene , biochemistry
Backgroud and purpose To study the anti‐atherosclerotic mechanisms of immune tolerance induced by Heat shock protein 60 (HSP60) Methods 40 male SD rats were randomly divided into healthy control group, atherosclerosis group (AS group), H1 group (oral HSP60 before modeling AS) and H2 group (oral HSP60 after modeling AS). The content of CD36, SR‐A, NF‐κB, HSP60 and regulatory T cells (Treg) in the aorta, lymph nodes and peripheral blood were detection by immunohistochemistry, flow cytometry, Western blot, PCR and ELISA. The intimal and vessel diameter ratios were calculated by the image analysis system. Results The levels of Treg cells in blood and lymphoid tissue increased. The pathological lesions of H1 group lighter than that of H2 group. The gene and protein expression of HSP60, SR‐A, CD36, NF‐κB in aorta of AS group were higher than that in the control group.The level of expression in the H1 group was lower than that in the H2 group. (P <0.05). Conclusion The immune tolerance induced by oral HSP60 could inhibit the arteries immune and inflammatory response, reduce the intimal injury and HSP60 antigen exposure and the degree of autoimmune response. Thereby it could also inhibit smooth muscle hyperplasia and maintain the stability of the fibrous plaques. Moreover, the earlier the oral HSP60, the better anti‐atherosclerosis effect.