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. 2012 Jun 22;303(5):L449–L459. doi: 10.1152/ajplung.00301.2011

Fig. 2.

Fig. 2.

Effect of ischemic acute kidney injury (AKI) on TNF-α levels and pulmonary TNF receptor (TNFR) 1 expression. A: serum TNF-α levels measured by ELISA (pg/mg) increased after kidney IRI at 2 h (20.1 ± 2.3 vs. 47.5 ± 6.9*, P = 0.04) and at 4 h (18.5 ± 2.5 vs. 56.4 ± 5.4*, P = 9.16 × 10−5), but not at 24 h (23.7 ± 4.3 vs. 38.6 ± 9.0, P = 0.16) compared with sham. B: lung tissue TNF-α levels did not increase after kidney IRI at either 4 h (51.6 ± 12.0 vs. 72.4 ± 7.2, P = 0.16) or 24 h (71.1 ± 23.5 vs. 51.6 ± 7.3, P = 0.47) compared with sham controls. C: RT-PCR confirmed no increase in lung TNF-α expression at either 4 (1 ± 0.1 vs. 0.98 ± 0.1, P = 0.5) or 24 (1 ± 0.3 vs. 1.1 ± 0.09, P = 0.6) h of ischemic AKI. n ≥ 5/group, D: relative fold change for WT lung TNFR1 gene expression by quantitative RT-PCR demonstrated increased expression at 4 h (FC = 1 ± 0.05 vs. 1.34 ± 0.11*; AV = 0.48 ± 0.02 vs. 0.65 ± 0.05*; P = 0.03) and 24 h (FC = 1 ± 0.19 vs. 1.81 ± 0.25*; AV = 0.41 ± 0.8 vs. 0.75 ± 0.1*; P = 0.03) compared with sham. *P < 0.05 vs. sham.