Figure 1.

L-Ascorbic acid (L-AA) eliminates sodium vanadate (SV)-induced cytotoxicity. (A) Western blots showing survival motor neuron (SMN) expression in SMN2-NSC34 cells treated with 400 μM L-AA, 200 μM SV, or SV combined with L-AA at different time points. β-Actin was used as an internal control. (B-D) Quantification of SMN protein expression in (A). (E-G) Quantification of the viability of SMN2-NSC34 cells (E) and human dermal fibroblasts (HDFs) (F, G) treated with L-AA, SV or SV combined with L-AA. (H, I) Western blots showing SMN and B cell lymphoma 2-associated X protein (Bax) expression in SMN2-NSC34 cells (H) and HDFs (I) treated with vehicle, L-AA, SV or SV combined with L-AA. β-Actin was used as an internal control. (J, K) Quantification of SMN and Bax expression in (H). (L, M) Quantification of SMN and Bax expression in (I). The experiment was repeated at least three times, and the mean ± SEM was calculated. Statistical comparisons were performed by one-way analysis of variance (ANOVA) (E-G) and Student's t test (B-D, and J-M).*P < 0.05, **P < 0.01, and ***P < 0.001.

Liu et al. BMC Medicine 2013 11:38   doi:10.1186/1741-7015-11-38
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