Figure 7.

Detoxification of acetaminophen (APAP)‐induced hepatotoxicity and renal injury by TPCD NP. a) Schematic illustration of the establishment of APAP‐induced organ toxicity and treatment regimens. b) Representative ex vivo images and quantitative analysis of Cy7.5/TPCD NP accumulation in the liver of mice at 12 h after administration. c,d) The levels of ALT and AST in serum collected from mice with APAP‐induced toxicity. e–g) The expression levels of TNF‐α, IL‐1β, and H₂O₂ in the hepatic tissues. h) The organ index of kidney. i,j) The serum levels of CREA and UREA. For therapy studies, at 6 h after i.p. stimulation with APAP at 200 mg kg⁻¹, mice were treated with different formulations. Mice in the normal group were not challenged with APAP. The model group was administered with saline. TPCD NP at 1.0 mg kg⁻¹ contained the same dose of the Tpl unit as that of the free Tpl group. At 12 h after different treatments, animals were euthanized and serum was collected for quantification of biochemical markers. Additionally, the liver tissues were isolated for quantification of inflammatory mediators. Data are mean ± SE (b, n = 3; c–j, n = 6). Statistical significance was analyzed by one‐way ANOVA with post hoc LSD tests. *P < 0.05, **P < 0.01, ***P < 0.001.