Fig. 7. Celastrol suppressed HCV NS5B induced inflammatory response in vivo depending on HSP90β.
C57BL/6 J mice were injected with pAde-EGFP or pAde-NS5B at 1 × 109 p.f.u./mouse through the tail vein (i.v.). Celastrol was intraperitoneally (i.p.) injected 48 h after pAde injection at the dose indicated on the figure twice a day continuously for 5 d. a Mice liver sections were stained with H&E and Masson’s trichrome staining. b Mice liver sections with stained with antibodies against CD68, Nlrp3, Hsp90α, and Hsp90β. Serum levels of (c) AST, (d) ALT, (e) Ifn-γ, (f) Mcp-1, and (g) Il-1β. mRNA expression levels of (h) Itga1, (i) Gdf15, and (j) Col1a1 in the liver. C57BL/6 J mice injected with pAde-NS5B alone or together with pAde-HSP90β A47S were treated with celastrol as in (a). Serum levels of (k) Ifn-γ, (l) Mcp-1, and (m) Il-1β. The results are representative of three independent experiments, data in (c–m) are presented as mean ± SEM (*P < 0.1; **P < 0.05; ***P < 0.01; n.s. not significant). n ≥ 5 mice in each group. Scale bar = 100 µm.