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. Author manuscript; available in PMC: 2009 Jul 1.
Published in final edited form as: Toxicol Sci. 2008 Apr 15;104(1):218–227. doi: 10.1093/toxsci/kfn079

Table 2.

Disruption of Keap1 and CDDO-Im pretreatment inhibits hepatic inflammation following ConA administrationa.

Genotype or Pre-treatment Treatment Macrophagesb Neutrophilsb Ifnγc Tnfαc Mip-2c Mcp-1c
cKeap1-WT Veh 2.6 ± 0.2 1.6 ± 0.1 16.0 ± 5.2 10.2 ± 0.6 102.3 ± 56. 7 29.1 ± 3.9
ConA 19.2 ± 1.9 * 14.5 ± 0.5 *

cKeap1-KO Veh 2.6 ± 0.2 1.7 ± 0.2 1.4 ± 0.4 ** 2.8 ± 1.3 ** 1.4 ± 0.7 ** 2.7 ± 1.2 **
ConA 8.1 ± 0.2 ^ 2.4 ± 0.4

Nrf2-WT + Veh Veh 3.2 ± 0.2 1.0 ± 0.1 18.2 ± 5.4 26.0 ± 3.3 286.6 ± 87.5 66.1 ± 10.6
ConA 16.3 ± 1.2 * 8.1 ± 0.7 *

Nrf2-WT + CDDO-Im Veh 2.5 ± 0.3 0.9 ± 0.1 1.5 ± 0.4 2.5 ± 0.6 1.1 ± 0.2 2.4 ± 0.3
ConA 4.8 ± 0.3 ^ 1.1 ± 0.2
a

Livers were harvested 24-hr following ConA administration. Values represent the mean ± SE (Nrf2-WT, N = 5; cKeap1-KO/ cKeap1-WT; N = 3)

b

Data are expressed as cells/field

c

Gene transcript levels are expressed as relative fold-change (ConA/Veh)

*

p < 0.05 compared to all groups within genotype, ANOVA-SNK multiple comparisons

^

p < 0.05 compared to ConA treated group within genotype, ANOVA-SNK multiple comparisons

**

p < 0.05 compared to cKeap1-WT, Student’s t-test

p < 0.05 compared to Nrf2-WT + Veh, Student’s t-test