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Objective:To observe the expression of B7-H4 in experimental autoimmune myocarditis (EAM).Methods:BALB/c mice were randomly divided into 2 groups:the control group and the experimental group.The mice of experimental group were injected with myosin to establish EAM models , while the mice of control group were injected with complete Freund 's adjuvant and normal saline.All the mice were killed separately at the 14th,21st,30th and 45th day for lymphocyte proliferation assay ,hematoxylin-eosin staining,immunohistochemical staining and real-time PCR.Results:The inflammation infiltration of heart was most serious at the 14th and 21st day,then it was gradually relieved with time;the results of lymphocyte proliferation assay and real-time PCR were similar to that of the inflammation infiltration of heart ,which were in high level at the 14th and 21st day,and they were both higher than that of the control group ( P<0.05 );B7-H4 protein were only detected in the experimental group ,and it was constantly expressed during the whole experiment on the endothelium of heart with myocarditis.Conclusion:B7-H4 participates in the progress of EAM ,and it may be a new way of studying the mechanism of myocarditis.
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Objective To investigate the feasibility to establish experimental model of autoimmune myocarditis and to study the value of echocardiographic assessment of left ventricular structure and function.Methods Seventy-two male 6 weeks old Lewis rats were randomly divided into 3 groups:normal control group,negative control group and positive group.Positive group were immunized with porcine cardiac myosin at days 0,7,30.Results ①The positive group showed weight loss,increased heart weight and myocardial necrosis with inflammatory infiltration.②The development of experimental autoimmune myocarditis included acute,subacute and chronic stages.The left ventricular diameter,ventricular wall thickness,left ventricular fractional shortening and ejection fraction of positive group differed significantly from those of other two groups.Conclusions Lewis rats immunized with porcine cardiac myosin may be a desirable experimental model of experimental autoimmune myocarditis,echocardiography can evaluate changes of cardiac structure and function accurately.
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Objective To explored the role of CD40/CD40L and B7-1/CD28 interaction in the immunopathologic process of folic acid-induced nephropathy(FAN) and investigate the intervention effect of the anti-B7-1 monoclone antibody(B7-1mAb). Methods GD1 mice were administrated by i. p with FA only or co-treated with B7-1 mAb for the intervention study. Kidneys were harvested for immunohistochemical, Western blot assays and serum for renal function evaluation at day 1, 3,5, 7, 14 and 21. Results Continuous expression of CD40, B7-1 from day 1 to day 21 on the renal tubular epithelial cells was detected in this model. CD40 was up-regulated more than five times in the kidney at every test time point (P
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<p><b>OBJECTIVE</b>To investigate the increased podocyte permeability by evidence of adriamycin (AD) and its molecular mechanism.</p><p><b>METHODS</b>In this study, we explored the direct effects of AD on cultured mouse podocytes and the potential protection effects of Dexamethasome (Dex).</p><p><b>RESULTS</b>After 24-hour AD (5 x 10(-7) mol/L) treatment, albumin passage through podocyte monolayers was increased by 2.27-fold (P < 0.01). AD caused a 62% decrease in Zonula Occluden-1 (ZO-1) protein (P < 0.05), suggesting that AD might increase podocyte permeability by disrupting tight junctions. Dex (1 x 10(-6) mol/L), co-administered with AD, protected podocytes from AD-induced increased albumin passage. This may be linked with an increased P-cadherin protein level to 1.93 fold of control (P < 0.01).</p><p><b>CONCLUSIONS</b>AD has a direct, detrimental effect on podocyte permeability, probably through disrupting tight junctions; Dex could protect against AD-induced high podocyte permeability by upregulating adherent protein P-cadherin.</p>