Figure 2
Figure 2. CO attenuates IL-6–induced STAT-3 activation. (A) HepG2 cells were treated with IL-6 (10 ng/mL) in a time-dependent manner, and then total cell lysates were probed with Ab for tyrosine phosphorylated or total STAT-3. Cells were preincubated for 2 hours with CORM-2 (20μM) and were then exposed for 30 minutes to IL-6 (B,D). (C) HepG2 cells were transiently transfected with STAT-3 DN vector, STAT-3 wild-type vector, or empty vector and exposed to 10 ng/mL of IL-6 for 18 hours in the presence or absence of CORM-2. Cells were transiently transfected with siRNA against human SOCS-3. After transfection, the cells were incubated with CORM-2 and then exposed to IL-6 for 30 minutes (E) or 18 hours (F). Values are means ± SEM from 3 independent experiments. *P < .05; **P < .01; ***P < .001.

CO attenuates IL-6–induced STAT-3 activation. (A) HepG2 cells were treated with IL-6 (10 ng/mL) in a time-dependent manner, and then total cell lysates were probed with Ab for tyrosine phosphorylated or total STAT-3. Cells were preincubated for 2 hours with CORM-2 (20μM) and were then exposed for 30 minutes to IL-6 (B,D). (C) HepG2 cells were transiently transfected with STAT-3 DN vector, STAT-3 wild-type vector, or empty vector and exposed to 10 ng/mL of IL-6 for 18 hours in the presence or absence of CORM-2. Cells were transiently transfected with siRNA against human SOCS-3. After transfection, the cells were incubated with CORM-2 and then exposed to IL-6 for 30 minutes (E) or 18 hours (F). Values are means ± SEM from 3 independent experiments. *P < .05; **P < .01; ***P < .001.

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