Fig. 4: Hyperglycemia induces ROS production in KC in response to APAP-mediated acute liver injury. | Cell Death Discovery

Fig. 4: Hyperglycemia induces ROS production in KC in response to APAP-mediated acute liver injury.

From: Hyperglycemia exacerbates acetaminophen-induced acute liver injury by promoting liver-resident macrophage proinflammatory response via AMPK/PI3K/AKT-mediated oxidative stress

Fig. 4: Hyperglycemia induces ROS production in KC in response to APAP-mediated acute liver injury.

Mice were subjected to STZ pretreatment and APAP administration as described in “Materials and methods” section. KCs were isolated from different experimental groups. a ROS production was detected by CarboxyH2DFFDA in KCs (original magnification ×200). Representative of three experiments. Positive green fluorescent-labeled cells were counted blindly in 10 HPF/section (×200). b Quantification of ROS-producing KCs (green) per high power field (×200) (n = 3/group). Both CON and STZ mice were pretreated with ROS antagonist NAC or saline in vivo prior to APAP treatment. c KCs were isolated from different experimental groups. ROS production was detected by CarboxyH2DFFDA in KCs (original magnification ×200). Representative of three experiments. Positive green fluorescent-labeled cells were counted blindly in 10 HPF/section (×200). d Quantification of ROS-producing KCs (green) per high power field (×200) (n = 3/group). e Isolated KCs from different experimental groups were cultured for 6 h, and TNF-α, IL-6, and IL-10 protein were measured in the culture supernatant by ELISA (n = 3/group) (mean ± SD, *p < 0.05)

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