Establishment And Inlfammatory Mechanism Research Between IgAN And Chronic Periodontitis In Rats

Objective:To analyse the possible correlation and inflammation mechanism betweenIgA nephropathy （IgAN） and chronic periodontitis （CP） by establishing chronicperiodontitis and IgA nephropathy stack animal model in SD rats.Methods：Eighty healthmale SD rats weighing200-240g were randomized into four groups（20pes/group）,A（control group）,B（IgAN group）,C（CP group）,D（CP accompany with IgAN group）,20Rats in every group.Established CP model by ligating silk suture and besmearedpathogenic bacterium in rats dental cervix;Using bovine serum albumin（BSA）+lavageinjection lipopolysaccharide（LPS）+carbon tetrachloride（CCl4）method to establishexperimental IgAN model.Ten rats were sacrificed respectively in every group at the endof week8and12,the blood, urine, kidney tissue samples were examined.The observationindex:general situation,proteinuria,hematuria,kidney and liver function,renal tissuepathology.The expression of MCP-1、IL-6in serum and nephridial tissue were examinedby ELESA and immunohistochemistry method.The severity CP and CRF was quantifiedby histopathology. The data were statistically analyzed.Results:The correlated detectionrevealed CP and IgAN animal models were established successfully.Renal functionrevealed that Renal function revealed that Scr and BUN in group A、B、C was not obviousdifference,but that in group D was higher than the third group（P﹤0.05）at8weeks, to12weeks group the differences between group B and A、C were significant（P＞0.05）andthat in group D was higher than group C（P=0.000；P=0.000）;Eight weeks B,C,D groupof24h urine protein content were higher than that in group A（P﹤0.05）,to12weeks B and C group comparison difference was not statistically significant（P=0.703）,butcompared group D （P=0.000）;8weeks B and D group appear microscopichaematuria,about75%of macroscopic haematuria,to12weeks B and D rats,microscopically red blood cell count,increasing group D group B is significant, and Acomparison group were statistically significant（P<0.05）;renal pathology showed:At8weeks, basic normal glomerular morphology in rats of group A,rat glomerular occasionalmild mesangial broadening, renal interstitial had mild hyperplasia of fibrous tissue in ratsof group B,group D significantly heavier than group B,both A focal varying degreesglomerular mesangial proliferation hardening,glomerular mesangial significantlybroadening,focal segmental sclerosis, with diffuse or focal inflammatory cell infiltration inD group at the end of week12,PAS score differences between group A and group C has nostatistical significance（Z=0.669，P=0.503）,group D was higher than group B（Z=2.803，P=0.005）.Obvious inflammation of periodontal tissue was observed in group C and D,and MBI were higher than that in group A and B,D group is significantly higher than Cgroup （Z=2.839，P=0.005）.The level of serum IL-6in group C and D were higher thanthat in group A and B（P﹤0.05）,And in group D was higher than that in group C（P﹤0.05）,The expression of MCP-1in nephridial tissue were compatible with that levels ofserum. B and D group express no obvious difference,D group is obviously higher than thatof the groupC（z=2.633，P=0.008）.Conclusion：This experiment can build fast, stable andreliable IgA nephropathy with periodontitis compound model, model success12weeks isbetter than the8weeks; Chronic periodontitis can be aggravating inflammatorymechanism of IgA nephropathy renal pathological damage.