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. 2004 Jan;24(1):36–45. doi: 10.1128/MCB.24.1.36-45.2004

FIG. 5.

FIG. 5.

PrxI expression at the early phase of carrageenan-induced pleurisy depends on both 15d-PGJ2 and Nrf2. (A) Both the COX-2 inhibitor NS-398 and nrf2 gene disruption affect PrxI expression during carrageenan-induced pleurisy. Whole-cell extracts of pleural inflammatory cells from wild-type mice (lanes 1, 3, 6, 9, 12, and 15), nrf2−/− mice (lanes 2, 4, 7, 10, 13, and 16), or NS-398-treated wild-type mice (lanes 5, 8, 11, 14, and 17) at the indicated time points of pleurisy were examined by immunoblotting with anti-PrxI antibody. (B) The expression of PrxI, 15d-PGJ2, F4/80, HO-1, COX-2, and hematopoietic PGDS in pleural inflammatory cells at 24 h of pleurisy was analyzed immunohistochemically with the corresponding antibodies as indicated. Arrows indicate macrophages, while arrowheads represent neutrophils. (C and D) Administration of NS-398 affects neutrophil (C) and macrophage (D) numbers during carrageenan-induced pleurisy. The number of pleural inflammatory cells was microscopically counted, and the means from four experiments are presented with standard errors of the mean. *, significantly different from time-matched NS398-untreated mice (P < 0.05). a, significantly different from carrageenan-untreated wild-type mice at the 0-h time point (P < 0.05). b, significantly different from carrageenan-untreated nrf2−/− mice at the 0-h time point (P < 0.05). (E) Effect of indomethacin on pleural inflammatory cells. Cell counts were taken at 24 h of pleurisy. The means from four experiments are presented with standard errors of the mean. *, significantly different from untreated control mice (P < 0.05).