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. 2010 Feb 11;107(9):4188–4193. doi: 10.1073/pnas.0912263107

Fig. 5.

Fig. 5.

AL-LC activates programmed cell death through a p38α MAPK-dependent mechanism. (A) Increased apoptosis as determined by TUNEL assay in isolated cardiomyocytes incubated with AL-LC for 48 h relative to vehicle or Con-LC treatment. Coincubation of AL-LC with MnTMPyP (50 μM), a MnSOD mimetic, reduced cellular apoptosis. (B) AL-LC–induced apoptosis was prevented by inhibition of p38 MAPK with SB203580 (5 μM). (C) AL-LC enhanced Bax/Bcl2 expression ratio, which was prevented by treatment with SB203580. (D) AL-LC–induced apoptosis was inhibited by adenovirus-mediated overexpression of dominant negative p38α (p38αDN) but not dominant negative p38β (p38βDN). Bar graph data are means ± SE, each from three independent experiments. * and #, P < 0.05 vs. corresponding vehicle and Con-LC, respectively; †, P < 0.05 vs. AL-LC treated cells without MnTmPyP (A), SB203580 (B and C), as well as with vehicle or LacZ (D). (E) i.v. administration of AL-LC for 7 days increased cardiac tissue Bax/Bcl2 expression ratio in wild-type (WT) mice but not in DNp38αTG mice. n = 3 for each group, *, P < 0.05.