Fig. 2: Deletion of BRISC potently protects mice from D-GalN/LPS-induced fatal hepatitis. | Cell Death & Disease

Fig. 2: Deletion of BRISC potently protects mice from D-GalN/LPS-induced fatal hepatitis.

From: BRISC is required for optimal activation of NF-κB in Kupffer cells induced by LPS and contributes to acute liver injury

Fig. 2

A Survival rate of WT and Abro1−/− mice or Brcc3−/− mice after intraperitoneally injected with a lethal dose of D-GalN (700 mg/kg) plus LPS (15 μg/kg) (N = 10–11). Log-rank test. WT and Abro1−/− mice or WT and Brcc3−/− mice were treated with a sublethal dose of D-GalN (700 mg/kg) plus LPS (10 μg/kg) or PBS for 6 h (N = 3–6). B Serum levels of ALT and AST of WT and Abro1−/− mice or Brcc3−/− mice. Representative hematoxylin and eosin (H&E) staining of liver sections from C WT and Abro1−/− mice or D WT and Brcc3−/− mice. Necrotic area was shown as a percentage of the total field area. Representative images of TUNEL-stained liver sections of E WT and Abro1−/− mice or F WT and Brcc3−/− mice. TUNEL-positive cells per field were counted. G Representative liver sections of WT and Abro1−/− mice that were stained with cleaved caspase-3. Cleaved caspase-3 positive hepatocytes in each field were counted. Scale bar, 50 μm. Data are presented as mean ± SEM; *P < 0.05, **P < 0.01, ***P < 0.001; two-tailed unpaired t-test.

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