| BACKGROUND: Atherosclerosis is the pathological process caused by cardiovasculardisease, cerebrovascular disease, has become the first life-threaten of human beings, as highdisability and high mortality rate, it affects people’s normal life seriously. Currently there area variety of claims for the mechanism of occurrence and development of atherosclerosis,however only smoking, hypertension, diabetes and hyperlipidemia roles as definite clinicalevidence of atherosclerosis. But the exact pathogenesis remains to clear. While, mostscholars believe that the major mechanisms for the formation and the development processof atherosclerosis is the inflammation response and autoimmune.Mucosal tolerance is a specific suppression of cellular and/or humoral immuneresponses to an antigen by administration of the antigen via a mucosal surface. It is a form ofperipheral tolerance that evolved to treat external agents that gain access to the body via anatural route and usually achieve by oral route.With oral related antigen to cell antigen ofmucous membrane of the tolerance is a special kind of cellular immunity and humoralimmune tolerance, as a special form of peripheral immune tolerance.Oral immune tolerancehas been widely used in clinic, such as multiple sclerosis, rheumatoid arthritis and type1diabetes treatment. As a simple and effective, non-toxic, the method of clinical medicalworkers currently has been widely accepted.As a simple and effective, non-toxic, the methodof clinical medical workers currently has been widely accepted. Heat shock protein60confirmed by a large number of experiments in the immune response associated withatherosclerosis as antigen induced effect. Thus through oral oral immune tolerance to heatshock protein60for atherosclerosis role of antagonism may atherosclerosis treatmentprovides a new direction for the future.When low dose antigen in oral, immune tolerance cause intestinal regulatory T cellactivation after intestinal. Participate in immune regulation was the main function ofRegulatory T cells (regulatory T cell,Treg), it has the functions of low immune responseand immune suppression. Mainly by secrete interleukin10(IL-10) and transforming growthfactor β (TGF-β) and interleukin4(IL-4) to play a role of inhibition. Interleukin10and/ortransforming growth factor β has inhibition, immune inhibitory effect of chemotactic factor and the production of inflammatory cytokines, thus inhibiting the body’s own immuneresponse. In addition, interferon γ(IFN-γ) as main cells in the body inflammation factor,which can further promote inflammation, experiments have confirmed, IFN-γand itsreceptor defects ApoE knockout mice not to atherosclerosis, instead IFN-γ or its releasingfactor injection of IL-12and IL-18, can obviously increase the atherosclerosis of ApoEknockout mice. IL-10has immune inhibitory effect to T helper cell subsets1(Th1), andinhibit the production of Th1to IFN-γ, eventually inhibit atherosclerosis formation.OBJECTIVE: Heat shock protein（HSP）is a kind of cell stress protein. It come upoxidation stress inflammation reflects that make the stress protein synthesis increase, whencoronary arteries endothelial cell damaged. Heat shock protein60(HSP60), recently, wasmuch attentioned especially close relations with cardiovascular disease. In recent researchesshows that the mechanism of coronary atherosderosis has relation with immune reflect.Through the oral tolerance (OT), it can inhibit the inflammation of the heat shock protein,thus inhibiting coronary artery atherosderosis patch formation and progress. Through theanimal test, the aim of this study was to discover the method of oral tolerance is expected toprovide new targets for the treatment of coronary heat disease, and provide new basis forprevention of it.METHOD: Select the lipoprotein E knockout (ApoE-/-) mice, total of24only, malemice for7weeks, weight18to20grams, divided into HSP60group, High Fat group andControl group randomly.After treatment, respectively, raised12weeks, then put them to death. Formaldehydefixed the aortic root, then pathological, dyeing, observation compare arterial plaque area.Blood after centrifugation, frozen preservation, then apply ELISA enzyme league immunemethod to detect blood level of cytokines, including transforming growth factor β1,interleukin-10-and interferon γ.RESULT:The plaque area of the aortic root is: through pathology image analyzer, HSP60groupplaque area of the lumen area percentage can be relatively High Fat group decreased by33.52%(P <0.01).Determination of serum cytokine levels:1) The HSP60group serum interleukin10(IL-10) and transforming growth factor β1(TGF-β1) concentrations were significantly higher than High Fat group.(P <0.01); 2) HSP60group serum interferon γ (IFN-γ) concentrations were significantly lowerthan the High Fat group.(P <0.05).CONCLUSION:1, Through oral HSP60may establish immune tolerance animal models.2, Oral HSP60can increased the expression of IL-10and TGF-β1by regulatory the Tcells, play the role of resistance to atherosclerosis.3, Oral HSP60bring down the levels of IFN-γ, may be due to the TGF-β1and IL-10cut1(Th1) helper T lymphocytes subgroup.We wish it can provides a new method though the heat shock protein60by mouthinduced immune tolerance to prevent the occurrence and development of atherosclerosis... |
PDF Full Text Request