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. Author manuscript; available in PMC: 2010 Feb 1.
Published in final edited form as: Free Radic Biol Med. 2008 Oct 31;46(3):406–413. doi: 10.1016/j.freeradbiomed.2008.10.037

Fig. 3.

Fig. 3

Levels of TNF-α, inducible nitric oxide synthase (iNOS) and activated p38 MAPK and JNK. (A) Western blot analysis of tumor necrosis factor (TNF)-α levels in liver homogenate subjected to 18% sodium dodecyl sulfate polyacrylamide gel electrophoresis (SDS-PAGE). Precursor of TNF-α (25 kD) is shown, *P<0.05, #P<0.01, vs. control mice. (B) Western blot analysis of iNOS levels in liver homogenate subjected to 8% SDS-PAGE. *P<0.05, vs. control mice. (C) Western blot analysis of phosphorylation of p38 MAPK. Liver homogenate subjected to 10% SDS-PAGE and immunoblotted with rabbit anti-p-p38 (Thy 180/Tyr 182) and p38 (H-147) antibodies as described in Materials and Methods. *P<0.05, vs. control mice. (D) Western blot analysis of c-Jun N-terminal kinase (JNK) with rabbit anti-JNK1 (C-17) and mouse anti-p-JNK (G7) antibodies. Anti-p-JNK (G7) antibody can react with phosphorylated JNK1, JNK2 and JNK3 at Thr-183 and Tyr-185. *P<0.005, vs. control mice. Numbers under the blot refer to the mean ± SD of the ratio of TNF-α, iNOS to β-actin, pp38 to p38, p-JNK2 to JNK2 from 3 mice in each group.

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