Objective: To explore the molecular mechanism of chronic kidney disease(CKD)induced by periodontitis(CP)in rats through the inflammatory pathway mediated by NF-κB.Methods: 80 male SD rats were randomly divided into the control group,CP Group,CKD group,and CP + CKD group.ligating the maxillary second molar root and smearing bacteria to made CP model.CKD model was made by 5/6 nephrectomy.CP + CKD group:made CP and CKD models at the same time,but not in the control group.In the 12 th week,serum IL(interleukin,IL)-1β and TNF-α(tumor necrosis factor-α)was measured by ELISA.At the 12 th week of modeling,the renal tissues and the maxillary second molars were taken out after the rats were killed.We used PCR method to detecte the relative expression of NF-κB m RNA,and Western blot method to detecte the relative expression of phosphorylated NF-κB p-65.Results: After 8 weeks of modeling,24-hour urine protein quantity in CP Group [(11.25±5.21)mg/L],CKD Group [(19.00±8.21)mg/L],CP+CKD Group [(27.78±10.29)mg/L] are higher than that in control group [(3.45±3.08)mg/L](P<0.05);and CKD group,CP + CKD group are higher than that in CP Group(P<0.05);CP+CKD group is higher than that in CKD group(P<0.05).After 12 weeks of modeling,the levels of IL-1 β and TNF-α in CP Group [(70.15±8.93),(6.97±2.31)ng/L],CP+CKD Group [(75.17±12.81),(7.50±2.25)ng/L] are higher than those in CKD Group [(58.71±5.90),(6.01±1.41)ng/L](P<0.05),and the CKD group is higher than the control group[(43.95±4.89),(4.36±0.64)ng/L](P<0.05).There is no statistical significance in the relative expression of NF-κB m RNA in the four groups: control group(1.02 ± 0.25),CP Group(1.13±0.21),CKD Group(1.00±0.22),CP+CKD Group(0.91±0.16)(P>0.05).The relative expression of p-p65 protein in CP+CKD Group[(0.75±0.01)mg/L] is higher than that in control group(0.51±0.01),CP Group(0.55±0.02),CKD Group(0.61±0.03)(P<0.05),but there are no significant difference among control group,CP Group and CKD group.In the 12 th week of modeling,the pathological changes of renal tissue in the four groups are as follows: control group,CP Group: HE,PAS and Masson staining show that the renal tissue structure is basically normal.CP+CKD group and CKD group: HE staining shows glomerular atrophy and sclerosis,renal tubule atrophy disappeared or cystic dilatation,renal interstitial fibrosis,a large number of inflammatory cells focal or diffuse infiltration;PAS staining shows a significant widening of glomerular Mesangial matrix in both groups;Masson staining shows a large number of renal interstitial fibrous tissue hyperplasia,some peri-glomerular fibrosis,local interstitial fibrosis and chronic inflammatory cell infiltration in CKD group.In CP+CKD group,a large number of fibrous tissue hyperplasia,some glomerular and peri-glomerular fibrosis,interstitial fibrosis,partial renal tubule atrophy or dilation,structural disorder,a large number of chronic inflammatory cell infiltration.The degree of renal lesion in CP+CKD group is severe than that in CKD group.The pathological changes of the periodontal tissues of the second maxillary molars in the four groups are as follows: the HE staining of the periodontal tissues in the control group and CKD group are basically normal.In CP+CKD Group and CP group,we observed the loss of gingival attachment and the formation of periodontal pocket: a large number of inflammatory cells infiltrated subcutaneously in gingival epithelium accompanied with the proliferation of fibrogranulation tissue;part of alveolar bone is damaged and absorbed,bone marrow cavity is vacuolated and cementum is damaged.Compared with CP group,the lesions in CP + CKD group is serious.Conclusions: CP can promote the expression of IL-6 and TNF-α in serum by activating NF-κB signaling pathway,cause aggravation of the renal pathological manifestations of CKD. |