Protective effect of puerarin on endothelial dysfunction of heat shock protein 60 induced specific immunity in apolipoprotein E-null mice.
- Author:
Da-zhu LI
1
;
Ying-feng HU
;
Ke-ping YANG
Author Information
- Publication Type:Journal Article
- MeSH: Animals; Anti-Inflammatory Agents; pharmacology; Apolipoproteins E; genetics; B7-2 Antigen; immunology; Cell Proliferation; drug effects; Chaperonin 60; metabolism; Dendritic Cells; drug effects; enzymology; immunology; Endothelium, Vascular; drug effects; physiology; Immunity; drug effects; Inflammation; chemically induced; Isoflavones; pharmacology; Mice; Mice, Inbred C57BL; Mice, Knockout; Protective Agents; pharmacology; T-Lymphocytes; drug effects; Vasodilator Agents; pharmacology
- From: Chinese Journal of Integrated Traditional and Western Medicine 2006;26 Suppl():4-6
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo investigate the influence of endothelial dysfunction induced by inoculated dendritic cells (DCs) loaded heat shock protein 60 (HSP60) in apolipoprotein (Apo) E-null mice, and the effect of Puerarin on it.
METHODSHSP60 DC (DChsp) acquired after prepared bone marrow-derived DCs of ApoE-null mice and treated with HSP60. In vitro, the function of DCs and the effect of Puerarin were detected. While in vivo, ApoE-null mice fed with high-cholesterol forage were divided into two groups and intravenous inoculated with DCh-sp or normal saline via vein twice respectively. The mice in the two groups were subdivided into the Puerarin group and non-treated group, and they were injected intraperitoneally with Puerarin and normal saline at the beginning of inoculation and the following 3 weeks, respectively. In addition, C57BL/6 mice without inoculation were taken as the normal control group. Two weeks after the last time inoculated, the response of T lymphocytes to HSP60 and endothelial-dependent diastolic function of aortic ring were detected.
RESULTSHSP60 could promote DCs expressed CD86 and stimulate T lymphocytes proliferation in vitro, while Puerarin had significantly inhibitory effect. After inoculated, DChsp activated inflammatory response in vivo and aggravated endothelium-dependent dilation in mice. Puerarin could significantly inhibit inflammatory reaction caused by DChsp and improve endothelium dilation.
CONCLUSIONHsp60 could activate DCs in vitro and in vivo, Puerarin could significantly inhibit specific immunity induced by HSP60 and improve vascular endothelium-dependent dilation.