Fig. 6.

NAC treatment relieves oxidative stress-induced chondrocyte senescence and mitigates OA phenotypes in PTEN-deficient mice. a Representative images of safranin O staining of articular sections of knee joints from 10-month-old Ctrl and PTEN^fl/fl mice as well as PTEN^fl/fl littermates treated with NAC for 9 months (n = 12 per group). b Quantified pathological changes of each group shown in (a). Each value represents the mean ± SEM (n = 12 per group). **P < 0.01. c Representative images of OxyIHC staining of knee joints from each group shown in (a) (n = 3 per group). The framed area in each picture is shown below at a higher magnification. d OxyBlot analysis for protein oxidation and western blot analyses for the levels of p53, PTEN, p-Akt, and Akt in articular cartilage from 6-month-old Ctrl and PTEN^fl/fl mice as well as PTEN^fl/fl littermates treated with NAC for 5 months. Quantitative densitometry results are shown below. The GAPDH protein serves as an endogenous normalizer. e Representative images of SA-β-gal staining of articular cartilage from 6-month-old Ctrl and PTEN^fl/fl mice as well as PTEN^fl/fl littermates treated with NAC for 5 months (n = 3 per group). Arrows denote senescent articular chondrocytes. f Representative images of Col10a1 in situ hybridization analysis of knee joints from each group shown in (a) (n = 3 per group). g Representative real-time PCR analyses of Col10a1, Mmp13, and Mmp9 expression in articular chondrocytes from 1-, 5- and 10-month-old knee joints. NAC was administered every other day from 1 month to the time of sacrifice. Each value represents the mean ± SEM (n = 3 per group). **P < 0.01. Scale bars: 250 µm in (a) and (c), 50 µm in (e) and (f)