Research Paper Volume 13, Issue 14 pp 18879—18893

Myeloid DJ-1 deficiency protects acetaminophen-induced acute liver injury through decreasing inflammatory response

DJ-1 deficiency does not affect APAP metabolism and mitochondrial dysfunction both in vivo and in vitro. Fasted WT and DJ-1−/− mice were intraperitoneal injected with a single dose of 300 mg/kg of APAP. (A) GSH levels after APAP treatment (n = 3–5). (B) MDA levels after APAP treatment (n = 3–5). (C) HMGB1 levels after APAP treatment (n = 3–5). (D) Western blot analysis of CYP2E1 in liver tissues after APAP treatment. B-actin was used as control. (E) Isolated primary WT and DJ-1−/− hepatocytes were starved and treated with APAP. Representative images of mitochondrial membrane potentials in primary hepatocytes 6h after APAP treatment evaluated using JC-1 (origin magnification ×100) (n = 3). (F) Representative images of mitochondrial ROS in primary hepatocytes 6h after APAP treatment evaluated with the MitoSOX Red probe (origin magnification ×100) (n = 3). Data are shown as means ± SD.

Figure 3. DJ-1 deficiency does not affect APAP metabolism and mitochondrial dysfunction both in vivo and in vitro. Fasted WT and DJ-1−/− mice were intraperitoneal injected with a single dose of 300 mg/kg of APAP. (A) GSH levels after APAP treatment (n = 3–5). (B) MDA levels after APAP treatment (n = 3–5). (C) HMGB1 levels after APAP treatment (n = 3–5). (D) Western blot analysis of CYP2E1 in liver tissues after APAP treatment. B-actin was used as control. (E) Isolated primary WT and DJ-1−/− hepatocytes were starved and treated with APAP. Representative images of mitochondrial membrane potentials in primary hepatocytes 6h after APAP treatment evaluated using JC-1 (origin magnification ×100) (n = 3). (F) Representative images of mitochondrial ROS in primary hepatocytes 6h after APAP treatment evaluated with the MitoSOX Red probe (origin magnification ×100) (n = 3). Data are shown as means ± SD.