Figure 1 Oral P.g administration induces periodontitis and CKD.
(A) The animal model experimental design. (B) H&E staining of inflammatory cell infiltration in maxillary sections. (C) AfterP.g infection, body weight changes in the mice (N=12 in the experimental group, N = 12 in the control group, six males and six females in each group) were monitored weekly. (D) P.g increased creatinine and urea nitrogen levels in vivo . (E) Western blot showing that cystatin C was highly expressed in the P.g group. (F) Quantitative analysis of the Western blot results. The data are shown as the means ± SDs from 3 experiments. (G) ELISA results showing an increased level of urine proteins in the P.g group. (H) H&E staining showing tubular damage and inflammatory cell infiltration in the P.g group. (I) PAS staining. (J) Histogram showing RT‒PCR analysis of kgp, rgpA and rgpB mRNA expression in kidney tissues (n = 12 in the experimental group, n = 12 in the control group). (200× magnification; scale bar 100 μm) (*P<0.05 , vs. the control group). **P<0.01 , vs. the control group.)