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. 2019 Jul 23;20(3):2511–2518. doi: 10.3892/mmr.2019.10520

Figure 3.

Figure 3.

Sestrin2 alleviates LPS-injured cell viability and LPS-enhanced inflammatory response in cardiomyocytes. (A) Cell viability of the cardiomyocytes treated with LPS (5, 10 and 50 µg/ml) for 24 and 48 h were inhibited time-dependently. (B) Sestrin2 promoted LPS-inhibited cell viability of the H9c2 cells. (C) Sestrin2 reversed the LPS increase in CTnT levels. (D) Sestrin2 reversed LPS increase in TNF-α levels. (E) Sestrin2 reversed LPS increase in IL-6 levels. (F) Sestrin2 reversed LPS increase in MDA levels. **P<0.01 vs. the control group, #P<0.05 and ##P<0.01 vs. the Sestrin2 group, ^^P<0.01 vs. the siSestrin2 group, &P<0.05 and &&P<0.01 vs. the LPS group. LPS, lipopolysaccharide; CTnT, cardiac troponin T; MDA, malondialdehyde; IL-6, interleukin 6; TNF-α, tumor necrosis factor-α.