Fig. 6

UA alleviated CuONPs-induced vascular injury in mice. A Schematic figure for animal experiments. C57BL/6 J mice were treated with vehicle (PBS) or UA (30 mg/kg) for 1 week by intragastric gavage (i.g.), and then exposed to CuONPs via intratracheal instillation (i.t.), meanwhile the mice in UA group and CuONPs + UA group were continuously treated with UA (30 mg/kg) by gavage for 3 days. B Representative TEM images of mice abdominal aorta dissected from CuONPs-treated mice. Mice were intratracheally instilled with CuONPs (5 mg/kg) for 3 days. N, nucleus; C, cytoplasm; Mt, mitochondria; IEM, internal elastic membrane. C and D Western blotting analysis and quantification of protein levels of Fis1, TIM23, ATP5B and LC3B in mice aorta tissues. Mice were intratracheally instilled with 2.5 mg/kg or 5 mg/kg CuONPs for 3 days. Actin was used as the internal control. E Representative TEM images of mice abdominal aorta dissected from CuONPs-treated mice. Mice were treated with UA (30 mg/kg) for 10 days by intragastric gavage and then intratracheally instilled with CuONPs (5 mg/kg) at day 7. N, nucleus; C, cytoplasm; Mt, mitochondria; IEM, internal elastic membrane. F Western blotting analysis and quantification of protein levels of mitochondria related proteins in aorta tissues dissected from CuONPs-treated mice with or without UA. Actin was used as the internal control. G Western blotting analysis and quantification of protein levels of oxidative stress response proteins in aorta tissues dissected from CuONPs-treated mice with or without UA. Actin was used as the internal control. In C and D, two-tailed unpaired Student’s t test was performed for statistical analysis. In F and G, one-way ANOVA with Tukey’s test was used for multiple comparisons. Results are representative of at least three independent experiments. Data are mean ± S.D. *p < 0.05