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. 2017 Oct 13;16(6):9521–9527. doi: 10.3892/mmr.2017.7789

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Copyright: © Ding et al.

This is an open access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made.

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Figure 3. — Caveolin-1 mediated oxidative stress-induced cellular senescence. (A) Caveolin-1 silencing induced a decrease in senescent cells when compared with NP-CTR, as determined by SA-β-gal staining. (B) Caveolin-1 silencing was associated with the recovery of proliferative ability. *P<0.05 vs. NP-CTR. SA-β-gal, senescence-associated β-galactosidase; NP, nucleus pulposus; t-BHP, tert-butyl hydroperoxide; NP-NOM group, cells cultured under normal conditions without t-BHP treatment; NP-CTR group, control cells treated with t-BHP only; NP-LV group, cells treated with t-BHP and lentivirus; NP-LV-NC, cells treated with t-BHP and negative control lentivirus.