Figure 6.

SGK1 inhibition intensifies inflammatory cell infiltration and modulates expression of TRAF3 and c-Jun in Porphyromonas gingivalis–infected gingival tissues. The 10- to 12-week-old C57/B6 mice were divided randomly into one sham control group and three experimental groups (n = 5 per group). The sham control group was treated with cellulose and 0.01% DMSO. The experimental groups were treated with P. gingivalis only, P. gingivalis with SGK1 inhibitor EMD638683 (15 mg/kg), or inhibitor only. Swabbing samples from the mouse oral cavity were examined by quantitative nested PCR to confirm P. gingivalis infection. A, the schematic flowchart showing the procedure of P. gingivalis–induced mice bone loss model. B, representative electrophoresis images showing P. gingivalis DNA obtained from oral samples. C and D, representative images of HE staining showing that P. gingivalis significantly increases inflammatory cell infiltration in gingival tissues, and SGK1 inhibition aggravates it. E and F, representative images of immunofluorescence staining showing that P. gingivalis increases infiltration of neutrophils, representing by the expression of Ly6G in gingival tissues (E), which is significantly increased with EMD638683 treatment (F). G–J, representative immunoblot images showing that EMD638683 significantly decreases expression of TRAF3 (G and H) but increases expression of c-Jun (I and J) in mice gingival tissues (n = 5 mice). H and J, the mean of ratio changes for TRAF3 and c-Jun, which were normalized to the sham control mice from each different group. The blots shown above are representative of five biological replicates. Error bars represent SD. ∗ and ∗∗∗ represent p < 0.05 and p < 0.001, respectively. DMSO, dimethyl sulfoxide; SGK1, serum- and glucocorticoid-regulated kinase 1; TRAF, tumor necrosis factor receptor–associated factor.