Journal: Antioxidants
Article Title: Nucleoredoxin Redox Interactions Are Sensitized by Aging and Potentiated by Chronic Alcohol Consumption in the Mouse Liver
doi: 10.3390/antiox13030257
Figure Lengend Snippet: Determination of DNA damage and cellular senescence markers induced by chronic alcohol consumption in the liver of young and aged mice. ( A ) IF analysis and signal quantification of PAR protein. Magnification is 20× and the scale bar indicates 100 μm. ( B ) Histochemical analysis and signal quantification of SA-β-gal activity. Magnification is 20 and 40×, and the scale bar indicates 50 μm. ( C ) WB analysis and intensity quantification of pH2A.X protein. pH2A.X protein levels were normalized with those of GAPDH protein, which was used as a loading control. ( D ) IHC analysis and signal quantification of IL-6 protein. Magnification is 20× and the scale bar indicates 50 μm. Bars represent the mean ± SE. * Significantly different from 7W, ** from 12M compared to the C group, * from 7W, ** from 12M compared to the ALD group, & from 7W, && from 12M, &&& from 18M compared to the respective control group; p < 0.05. n = 5 animals/group. ALD, alcohol liver disease model; C, control; 7W, 7-week-old mice; 12M, 12-month-old mice; 18M, 18-month-old mice.
Article Snippet: Next, for IHC analysis, primary antibodies against collagen 3 alpha 1 (COL3A1; 1:200; NB600-594SS, Novus Biologicals; Centennial, CO, USA), interleukin 6 (IL-6; 1:100; 21865-1-AP; Proteintech; Rosemont, IL, USA), KI67 and collagen 1 alpha 1 (KI67; 1:200 and COL1A1; 1:200; GTX16667 and GTX112731, respectively; GeneTex; Irvine, CA, USA), were incubated overnight at 4 °C in the blocking solution provided in the kit (MM510; BioCare Medical).
Techniques: Activity Assay, Control