Fig. 1: The knockdown of AIM2 exacerbates APAP-induced acute hepatic damage in mice aged 30–32 weeks. | Cell Death Discovery

Fig. 1: The knockdown of AIM2 exacerbates APAP-induced acute hepatic damage in mice aged 30–32 weeks.

From: AIM2 regulates autophagy to mitigate oxidative stress in aged mice with acute liver injury

Fig. 1

A Analysis of serum ALT and AST levels and B liver H&E staining in 8- and 24-h post i.p. injection of PBS or APAP in 8-week-old WT (n = 21) and AIM2−/− (n = 20) mice. PBS group n = 3. The liver H&E staining image is shown with a scale bar of 100 µm. AIM2 levels in the livers of WT mice (10, 20, and 30 weeks old) after APAP administration were quantified using C qPCR and D Western blotting. n = 4 mice per group. E Measurement of serum AST and ALT levels at each time point after i.p. injection of PBS or APAP in 30–32-week-old WT (n = 8) and AIM2−/− (n = 9) mice. PBS group n = 3. F, G display liver tissue H&E staining results after 8, 24, and 72 h of APAP administration. The extent of liver injury was quantified using Image J software. Each experimental group comprised 8–10 mice, and the experiment was repeated three times. The statistical analysis showed that AIM2 knockdown aggravated APAP-induced acute hepatic damage in mice (*P < 0.05; **P < 0.01; ***P < 0.001).

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