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. Author manuscript; available in PMC: 2009 Oct 1.
Published in final edited form as: Hepatology. 2008 Oct;48(4):1213–1223. doi: 10.1002/hep.22471

Figure 1.

Figure 1

Response of CXCR2-/- mice to ischemia/reperfusion. (A) Neutrophil accumulation was determined by liver content of myeloperoxidase (MPO) and scoring based on chloroesterase acetate staining. Data are mean ± SEM with n=4-15 per group. *P<0.05 compared with CXCR2-/- mice. (B) Liver injury was measured by serum levels of alanine aminotransferase (ALT). Data are mean ± SEM with n=4-15 per group. *P<0.05 compared with CXCR2-/- mice. (C) Liver histology. Normal hepatic architecture was observed in sham-operated wild-type mice and CXCR2-/- mice. After 12 or 24 hours of reperfusion, livers from wild-type mice had large areas of necrosis, whereas livers from CXCR2-/- mice showed less evidence of necrosis. After 48 hours of reperfusion, wild-type mice still had severe necrotic livers, whereas CXCR2-/- mice had significantly improved livers with small necrotic areas. After 96 hours of reperfusion, large necrotic areas remained in the livers of wild-type mice, whereas livers in CXCR2-/- mice were almost normal. Asterisks indicate necrotic areas. Original magnification was 50X.