Study On The Mechanism Of Oxidized LDL Induced CD40 Signaling In Cultured Human Umbilical Vein Endothelial Cells And The Protective Effect Of Captopril

Artherosclerosis is a chronic inflammation process of inflammation responding and fiber cell propagating for characteristic. Ox-ldl has the cell toxicity function, can stimulate cell creation various cytokine and growth factor, thereby promote the occurrence and development of artherosclerosis . Immunity factors have important role in the process of artherosclerosis formation and development, and CD40/ CD40 L leads important function in the activativity and humoral immunity of T cell and B cell . The interaction of CD40-CD40 L is an important path for delivering inflammation and immunity signal of lymphoid cells. Recent years CD40/ CD40 L is extensive to exsit in every kind of cell of artherosclerosis spot, its interaction showing affecting related cell in artherosclerosis , and is close correlation with spot piece related. Some researchs have confirmmed that recepters of ox-ldl lead the pathologic reaction of ox-ldl, the LOX-1 is scavenger receptor of main exsitting in vessel smooth muscle cell .Endothelial cells intaking ox-ldl through LOX-1 result the changes of structure and form endothelial cells. This experiment confirms that ox- LDL can cause the high expression of CD40 in endothelial cell, and assume Concentration- Dependence, after joining the LOX-1 blocking agent, the expression of CD40 decreased, the indirect elucidation that ox- LDL is activated the signal of CD40 by LOX-1, causes the inflammation responds and endothelial cell damage.NF- κ B regulates varieous cytokines participated in theinflammation responds, the immunity responds, cellproliferation and adjusts gene expression of glutinous molecul, inflammation medium, protease, thus controls their biosynthesize. It has confirmed that the activated NF- k B exsits in the human artherosclerosis spot includding the smooth muscle cell, macrophage , endothelial cells.Nitricoxide synthase can induse nitricoxide synthesizes,while nitricoxide is a kind of important living creature cytokine, it diastoles blood vessel and represses infro-cell glutinous molecu expressing, repressing xanthine oxidase producing, enhancing endothelial cells resisting ability. Angiotensin converting enzyme inhibitor ( ACEI) has the heart protection function, ACEI can repress the bradyknin activity , reducing the bradyknin degradation thus arouses the level of endogenetic bradyknin , endogenetic bradyknin stimulated the creation of prostacyclinI2( PGI2) and nitricoxide ( NO) through bradyknin B2 receptor. Bradyknin , prostacyclin and nitricoxide are important endogenetic heart protection material, diastoling coronary artery , repressing aggregation of leucocyte and platelets. In this experiment , expresses of CD40 in the NF- k B blocking agent groups are lower than that of ox- LDL groups(p<0. 05), confirmming ox-ldl activated the CD40 expression through NF- k. B in the inflammation process of endothelial cells . The expression of CD40 in the pre-giving captopril groups are lower than that of ox- LDL groups (p<0. 05). The expression of CD40 in the pre-giving PDTC, captopril , NAME groups is lower than that of ox- LDL groups( p<0. 001). The anti- AS function of Captopril may be lead the...