Figure 6
PVP-I inhibits inflammation in LPS-stimulated mice. (a) Nasal polyps mouse models protocol. Mice were assigned to 4 groups and administered saline or PVP-I at doses of 0.1% intra-nasally for on 7 days after LPS administration (intra-nasal) for 12 weeks. Nasal polyps mouse models protocol. Mice were assigned to 4 groups and administered PVP-I at doses of 0.1% intra-nasally or DEX at doses of 1 mg/kg intraperitoneally for on 7 days after 10 µg LPS intra-nasally for 12 weeks. (b) Representative hematoxylin and eosin staining to demonstrate nasal mucosa tissue. Statistical significance: *P < 0.05 compared with the control group; #P < .05 compared with the LPS + PBS group; §P < 0.05 compared with the LPS + DEX group. (c) Goblet cells increased in the epithelium with PAS staining upon LPS administration. In the epithelium, number of goblet cells of the LPS administration group was more than in the CON group and was further inhibited in the PVP-I treatment group. Statistical significance: **P < 0.01 compared with the control group; #P < 0.05 compared with the LPS + PBS group; §P < 0.05 compared with the LPS + DEX group. (d) Immunohistochemistry showing the TLR4 and MyD88 in the nasal mucosa of mice in each group. Statistical significance: *P < 0.05 compared with the control group; §P < 0.05 compared with the LPS + DEX group. (e) Cells lysate in murine nasal mucosa tissue were immunoprecipitation with anti- MyD88 and TLR4 antibody, and then immunoprecipitated proteins were detected using anti-TLR4 and anti-MyD88 antibodies. PVP-I was found to inhibit the TLR4 and MyD88 complex formation. Actin was used as a control for input.
