Fig. 2: PHZ-OH attenuates organ dysfunction in bacterial sepsis via inhibiting caspase-11 signaling. | Cell Death & Disease

Fig. 2: PHZ-OH attenuates organ dysfunction in bacterial sepsis via inhibiting caspase-11 signaling.

From: Novel 1-hydroxy phenothiazinium-based derivative protects against bacterial sepsis by inhibiting AAK1-mediated LPS internalization and caspase-11 signaling

Fig. 2

Survival curves of WT and Casp11−/− mice treated with saline or PHZ-OH (5 mg/kg) and subsequently challenged with cecal ligation and puncture (CLP, ligating 75% of the cecal) (A) or E. coli (ATCC 29522, 109 CFU per mice) (B); C–H WT and Casp11−/− mice were treated with saline or 5 mg/kg of PHZ-OH 30 min prior to a challenge of CLP (ligating 75% of the cecal) or not (six mice per group). The plasma, the lung and the liver were sequentially harvested 12 h after the challenge of CLP, and stored for further experiments. Variations of plasma-associated parameters including aspartate aminotransferase (AST) and alanine transaminase (ALT) (C), and blood urea nitrogen (BUN) and creatinine (CREA) (D); E Hematoxylin and Eosin (H&E) staining of the lung; Plasma levels of IL-1α and IL-1β (F), and TNFα and IL-6 (G); H Western blots showing caspase-11 expression and GSDMD cleavage in the liver (representative of six mice per group). Data are mean ± SEM of six mice in one experiment. *P < 0.05. ns, not significant. Scale bar = 50 μm.

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