Skip to main content
. Author manuscript; available in PMC: 2011 Nov 1.
Published in final edited form as: J Hepatol. 2010 Jul 17;53(5):918–926. doi: 10.1016/j.jhep.2010.05.015

Fig. 5. Inhibition of p110γ selectively inhibits bile salt-induced apoptosis in hepatocytes but does not alter the effects of independent apoptotic stimuli.

Fig. 5

HepG2-Ntcp cells were stimulated with DMSO, 20 μM TLC or 75 μM of TCDC or GCDC. The p110γ inhibitor AS604850 (2.5 μM) was added 30 min prior to stimulation. (A) Apoptotic cells were quantified morphologically after Hoechst staining. Rate of apoptosis was expressed as % of apoptotic cells. (B) In separate experiments, apoptosis in identically stimulated HepG2-Ntcp was determined by caspase-3/-7 activity (*p <0.05 vs. control, n = 3–6). (C) Rat hepatocyte cultures were treated with 50 ng/ml Fas ligand for 4 hours and apoptotic cells were determined morphologically. AS604850 was added at 2.5 μM 30 min prior to the addition of Fas ligand (n = 3). (D) HepG2-Ntcp cells were treated with 200 μM etoposide or 200 ng/ml TNFα plus 28 ng/ml actinomycin D for 4 h and apoptotic effects were quantified in caspase-3/-7 assays. Prior to stimulation, cells were treated with 2.5 μM AS604850 for 30 min (n = 3).