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. 2005 Nov 4;34(3):274–285. doi: 10.1165/rcmb.2005-0277OC

Figure 5.

Figure 5.

Figure 5.

Figure 5.

Pharmacologic caspase inhibition amplifies BHT/O2 ALI by enhanced necrotic cell death. (A) Klan-Meier survival curves of BHT/O2-treated mice. z-ASP cotreatment (100 μg/mouse intraperitoneally daily) during initial BHT/O2 exposure (BHT/O2 + z-ASP 75%, see Figure 5Ce) amplifies early acute lung injury histologically and results in death by Day 6 compared with DMSO vehicle 21% (n = 12) BHT/O2 d6 → 21% (n = 12) and vehicle + z-ASP d6 75% → z-ASP 21% (n = 5) (Log rank survival BHT/O2 + z-ASP 75% versus controls, P < 0.03; n = 10 per group). (B) Densitometric comparison of actin-normalized cleaved caspase-3 expression and representative Western blot of lung lysates from BHT/O2 d6 + z-ASP compared with BHT/O2 + vehicle treated animals. The data represent mean ± SEM; n = 3 per condition; *P < 0.05; **P < 0.001. (C) H&E (a, c, e) or TUNEL-positive cells (FITC filter) co-stained with DAPI to identify nuclei (b, d, f). Numerous TUNEL-positive cells are present in BHT/O2 d6 (d) and z-ASP cotreated lungs (f). DAPI, 4′6-diamidine-2-phenylindole-dihydrocholride; TUNEL, terminal deoxynucleotide transferase–mediated dUTP nick end-labeling. Images are representative of 10 high-power fields per lung; n = 3 per condition.