Beclin-1-induced increase in autophagy prevents liver injury from GalN/LPS. (a) Mice were infected with the control LacZ or beclin-1-expresssing rAAV and left untreated or treated with GalN/LPS (G/L) for 5 h. Total liver protein was immunoblotted for beclin 1, caspase-3 (Casp 3), caspase-7 (Casp 7), PARP and tubulin. Arrows indicate the procaspases (Pro), the cleaved caspase-3 (p17) and -7 (p30 and p19) forms, and intact (p115) and cleaved (p85) PARP. (b) Serum ALT levels at 5 h after GalN/LPS treatment (*P<0.02 as compared with control mice; n=7–11). (c) Histological grade of liver injury in the same mice (*P<0.0005 as compared with control mice; n=7–11). (d) Numbers of TUNEL-positive cells per high power field (HPF; *P<0.001; n=3). (e) Mitochondrial protein isolates from rAAV-infected mice untreated or treated with GalN/LPS (G/L) for 5 h and probed for truncated Bid (tBid), cytochrome c (Cyt c) and cytochrome oxidase (Cyt ox) as a loading control. (f) Immunoblots of cytosolic protein from the same mice immunoblotted for caspase-8 and the other indicated proteins. The procaspase and cleaved caspase-8 images are different exposures of the same immunoblot. Results are representative of two independent experiments