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

Figure 6

Paricalcitol pretreatment upregulated PGE₂ and EP4 expression and increased the interaction between PGE₂ and EP4 in mice kidney with IR injury. (a) PGE₂ was highly produced after IR injury compared with the sham-operated mice without paricalcitol. Paricalcitol further increased renal PGE₂ concentrations in mice kidney with IR, but cotreatment with paricalcitol and AH-23848 decreased the PGE₂ concentrations. (b) The representative staining of EP4 immunoreactivity showed that the cellular membrane expression of EP4 was increased in mice kidney with IR injury and was further enhanced after paricalcitol pretreatment. Original magnification ×400. Bar = 50 μm. (c) The representative image of immunofluorescence staining confirmed that EP4-positive staining was colocalized with the AQP-1 on the cellular membrane of proximal tubule in paricalcitol-treated mice with IR injury. Original magnification ×400. Bar = 20 μm. (d) Immunoprecipitation showed that PGE₂/EP4 complex formation increased in paricalcitol-treated mice kidney with IR injury compared to mice kidney with IR injury only and significantly decreased in IR injury cotreated with paricalcitol and AH-23848. (e) The concentration of renal TXB₂ was not significantly different between groups treated with and without AH-23848. versus sham group, versus IR group, and versus IR + Pari group; = 6–8 for each group.

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