Fig. 4.

Nox2, Rac1/2, and p47^phox deficiency inhibits hepatic secretion of TNF-α following partial lobar liver I/R. The indicated genetic strains were subjected to 60 min of partial lobar ischemia followed by 3 h of reperfusion. Blood was then harvested by cardiac bleeds and plasma was assessed for TNF-α levels. A: comparison of plasma TNF-α levels between Nox1 KO and Nox1 WT littermates. B: comparison of plasma TNF-α levels between C57 inbred mice with WT, NOX2 KO, or p47^phox KO genotypes. C: comparison of plasma TNF-α levels between NOX1/2 WT and NOX1/2 double-KO mice. D: comparison of plasma TNF-α levels between Rac1^flx/flx/Rac2-WT (Rac1-WT/Rac2-WT), Rac1^flx/flx/Rac2-KO (Rac1-WT/Rac2-KO), AlbCRE-Rac1^flx/flx/Rac2-WT (Rac1-KO/Rac2-WT), and AlbCRE-Rac1^flx/flx/Rac2-KO (Rac1-KO/Rac2-KO) mice. In all panels results depict means ± SE. The N independent animals are given in each graph. Statistically significant differences in A–D were determined by a 2-tailed Student's t-test (#P < 0.05, *P < 0.005; †P < 0.0005). Marked comparisons are between the WT and KO postreperfusion time points. E and F: quantitative RT-PCR for NOX1 (E) and NOX2 (F) mRNA from total liver RNA generated from WT, NOX2 KO, NOX1 KO, and NOX1/2 double-KO mice. GAPDH was used as internal control using ΔCt calculations for relative abundance. Values show means (± SE, N = 5 independent animals) relative abundance of NOX transcripts normalized to GAPDH transcripts as 2^{−(Nox:Ct − GAPDH:Ct)} values. Dotted lines indicate the background levels of detection.