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. 2017 Mar 29;2017:5031926. doi: 10.1155/2017/5031926

Figure 10.

Figure 10

Paricalcitol prevented inflammatory cell infiltration and suppressed the expression of inflammatory cytokines via an EP4-dependent pathway in mice kidney with ischemia-reperfusion (IR) injury. (a) The infiltration of CD3+- and F4/80+-expressing cells was examined by immunohistochemical staining. The number of CD3+- and F4/80+-positive cells was increased significantly in mice kidney with IR injury, and this increase was ameliorated by paricalcitol. AH-23848 cotreatment significantly reversed the effect of paricalcitol on inflammatory cell infiltrations into the ischemic kidney. Original magnification ×400. (b) RT-PCR analysis showed that the mRNA levels of RANTES, TNF-α, IL-1β, and IFN-γwere elevated in mice kidney with IR injury. Paricalcitol suppressed the IR-induced overexpression of these inflammatory cytokines and cotreatment with AH-23848 reversed all of these suppressive effects. P < 0.05 versus sham group, P < 0.05 versus IR group, and P < 0.05 versus IR + Pari group; n = 6–8 for each group. Bar = 50 μm.