Paricalcitol Pretreatment Attenuates Renal Ischemia-Reperfusion Injury via Prostaglandin E₂ Receptor EP4 Pathway

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. versus sham group, versus IR group, and versus IR + Pari group; = 6–8 for each group. Bar = 50 μm.

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