Additional Supporting Information may be found in the online version of this article.

HEP_26320_sm_SuppFig1.tif1717KSupporting Information Figure 1. Representative immunohistochemical staining for HMGB1 in hepatocytes (A/B) or infiltrating macrophages/monocytes (C/D) harvested from WT vs. ASC KO livers (6h of reperfusion after 90min of warm ischemia). Magnification ×400, n=3-4/group (*p<0.0001).
HEP_26320_sm_SuppFig2.tif1715KSupporting Information Figure 2. Histopathology of ASC-deficient livers at 90min of warm ischemia only (A) vs. 90min ischemia plus 6h reperfusion (B). Representative of n=3-5/group; Magnification ×200.
HEP_26320_sm_SuppFig3.tif649KSupporting Information Figure 3. BMMs from ASC KO or WT mice were cultured with rHMGB1 (1μg/ml) for 24h. The expression of cleaved caspase-1 and TLR4 was evaluated by Western blots. rHMGB1 supplement increased the expression of cleaved caspase-1/TLR4 (A), and IL-1β (B, p<0.01) in both ASC-deficient and WT groups, compared with BMM controls without rHMGB1 adjunct. Representative of three experiments.
HEP_26320_sm_SuppFig4.tif648KSupporting Information Figure 4. BMMs and liver tissue proteins were isolated from ASC KO and WT mice. HMGB1 expression was evaluated by Western blots. The baseline HMGB1 levels were decreased both in vitro (A) and in vivo (B) in ASC KO group, as compared with WT controls. Representative of three experiments.
HEP_26320_sm_SuppFig5.tif1715KSupporting Information Figure 5. Liver histopathology (A) and Suzuki's scores (B) in WT mice infused with rHMGB1 immediately at reperfusion (0.8mg/kg, i.p. after 90min of ischemia). Sham controls underwent the same procedure without vascular occlusion. Unlike in sham controls, treatment with rHMGB1 augmented hepatocellular injury in WT mice subjected to liver IR. Magnification ×200. Representative of n=4/group. (*p<0.0001).
HEP_26320_sm_SuppTab1.tif231KSupporting Information Table 1.

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