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. 2019 Nov 26;10(12):888. doi: 10.1038/s41419-019-2112-1

Fig. 4. PGK1 knockout activates Nrf2 signaling and protects osteoblasts from DEX.

Fig. 4

Stable OB-6 osteoblastic cells (a–g) or primary human osteoblasts (h–k) with the CRISPR/Cas9-PGK1 knockout construct (“ko-PGK1”) or the CRISPR/Cas9 sgRNA control construct (“sg-C”) were established, expression of listed genes (a, b, h) was shown. The relative NQO1 activity was also tested (c). Cells were further treated with or without DEX (1 μM) for applied time periods, cellular superoxide levels were shown (d); cell viability (e, i), death (f, j), and apoptosis (g, k) were examined by MTT, LDH release, and Histone-DNA ELISA assays, respectively. Expression of listed proteins was quantified, normalized to the loading control (a, h). Data were expressed as mean ± standard deviation (SD, n = 5). *p < 0.05 vs. “sg-C” cells with “Ctrl” treatment. #p < 0.05 vs. “sg-C” cells with DEX treatment. Experiments in this figure were repeated three times, and similar results were obtained.