The Change Of IgA Nephropathy Rat Intestinal Mucosal Immune Cells And The Regulation Of Rhein

Aim:By observing the Ig A nephropathy rat intestinal mucosal immune cells number and distribution of changes in knowledge about the role of mucosal immunity on the pathogenesis of Ig A nephropathy process,by comparing the changes of the mucosal immune cells of before and after the application of rhein discussed rhein prevention mechanism of Ig A nephropathy,providing theoretical basis for the clinical application of rhein.Methods:28 SD female rats were randomly divided into normal control group,Ig A nephropathy model group,the rhein prevention group and rhein in treatment group(n= 7).With bovine serum albumin(BSA)+ lipopolysaccharide(LPS)+ carbon tetrachloride(CCl4)combination of Ig A nephropathy model was constructed,rhein prevention group and rhein treatment group respectively before and after the modeling of rats with rhein suspension lavage.Rats were executed in 10 weekend,executed the day before to collect urine for 24 hours urinary sediment of red blood cell count and 24 hours urinary protein detection.Executed after part of the ileum by conventional HE staining,observing the intestinal mucosa pathological changes;Take part of the ileum and kidney tissues with liquid nitrogen preservation,OCT embedding,the kidney Ig A deposits by immunofluorescence method and ileum mucosa appears with immune histochemical methods CD3+ T cells,CD4+ T cells,CD20+ B cell and CD83+ dendritic cells.Square net test system was used to measure intestinal mucosa lamina propria dendritic cells and lymphocytes number density.Using statistical software SPSS17.0 comparison between groups of rats the differences and correlation between lamina propria dendritic cells and lymphocytes.Result:1.Ig A nephropathy model group rats urine test visible microscopic haematuria,24 h urine protein content increased which had green immunofluorescence staining visible renal cortical granule Ig A sedimentary fluorescence,rhein prevention and rhein therapy group significantly reduce the damage.2.Ig A nephropathy model group rats gut HE dyeing visible become shorter and wider,fluffy spacing increases,the central lacteals expansion,lamina propria is a large number of inflammatory cells and red blood cells in the connective tissue.Rhein prevention and rhein therapy group significantly reduce the damage.3.Each group can be seen in the rats ileum mucosa epithelial CD3+ T cell,lamina propria visible CD3+ T cell,CD4+ T cell,CD20+ B cell and CD83+ dendritic cells.4.Compared with normal control group,number density of the Ig A nephropathy rat intestinal mucosa lamina propria CD3+ T cell,CD4+ T cell,CD20+ B cell and CD83+ dendritic cells were increased(p < 0.05).Number density of Ig A nephropathy model group rats of intestinal mucosa lamina propria CD83+ dendritic cells and CD4+T cell were significantly correlated.Number density of CD4+ T cell and CD20+ B cell has high linear correlation.5.Compared with the model group Ig A nephropathy,number density of RH prevention group and RH treatment group in the rat intestinal mucosa lamina propria CD3+ T cell,CD4+ T cell,CD20+ B cell and CD83+ dendritic cells were reduced(p <0.05).Number density of RH prevention group rat intestinal mucosa lamina propria CD4+ T cell and CD20+ B cell has high linear correlation.Number density of RH treatment group in the rat intestinal mucosa lamina propria CD4+ T cell and CD20+ B cell were significantly correlated.Conclusion:1.Number density of the Ig A nephropathy rat intestinal mucosa lamina propria CD20+ B cell,CD4+ T cell and CD83+ dendritic cells increased,prompt the humoral immune active,may have been caused by the Ig A abnormal increased and deposited in the kidney.2 Ig A nephropathy rat intestinal mucosa lamina propria dendritic cells,CD20+ B cell and CD4+ T cell was significantly correlation,prompt interactions between lamina propria dendritic cells and lymphocytes in the intestinal immune regulation.3 After rhein application can partly recovere increase of the various abnormal immune cells,may be by inhibiting the function of dendritic cells and the interaction of immune cells to regulate the intestinal immune.