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.)