Copyright
©The Author(s) 2019.
World J Gastroenterol. Nov 28, 2019; 25(44): 6527-6540
Published online Nov 28, 2019. doi: 10.3748/wjg.v25.i44.6527
Published online Nov 28, 2019. doi: 10.3748/wjg.v25.i44.6527
Figure 4 Gasdermin D knockout dramatically eliminates inflammatory damage in the liver and improves survival in D-galactose/lipopolysaccharide-induced acute liver failure mice.
A: Survival curve; B: Changes in liver tissue appearance; C: Alanine aminotransferase, international normalized ratio, and blood ammonia in mice; D: Pathological examination of the liver by haematoxylin and eosin staining. Scale bars = 100 µm; E: Ishak score of the liver tissue pathology. Data are presented as the mean ± square error. aP < 0.05, bP < 0.01, and eP < 0.001. WT: Wild type; GSDMD-/-: Gasdermin D genetic knockout; D-Galn/LPS: D-galactose/lipopolysaccharide; PBS: Phosphate buffer saline; ALT: Alanine aminotransferase; INR: International normalized ratio; H and E: Haematoxylin and eosin.
- Citation: Li H, Zhao XK, Cheng YJ, Zhang Q, Wu J, Lu S, Zhang W, Liu Y, Zhou MY, Wang Y, Yang J, Cheng ML. Gasdermin D-mediated hepatocyte pyroptosis expands inflammatory responses that aggravate acute liver failure by upregulating monocyte chemotactic protein 1/CC chemokine receptor-2 to recruit macrophages. World J Gastroenterol 2019; 25(44): 6527-6540
- URL: https://www.wjgnet.com/1007-9327/full/v25/i44/6527.htm
- DOI: https://dx.doi.org/10.3748/wjg.v25.i44.6527