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. 2018 Jun 28;2018:3583921. doi: 10.1155/2018/3583921

Figure 2.

Figure 2

Low expression of 14-3-3η abolished the protective effect of Tanshinone IIA (TSN) preconditioning on lactate dehydrogenase (LDH) activity and cell viability in H9c2 cells subjected to anoxia/reoxygenation (A/R) injury. (a, b) Effects of TSN on the expression of 14-3-3η in H9c2 cells subjected to A/R injury by Western blot analysis. Untreated cells which served as the AD14-3-3η RNAi group were incubated with adenovirus containing 14-3-3ηsiRNA, and the AD-scrRNA group was incubated with empty adenovirus vector. β-Actin served as a loading control (a). Pretreatment with TSN increased 14-3-3η expression under A/R injury, which was silenced by AD14-3-3η RNAi (b). TSN pretreatment inhibited activity of LDH (c) and increased cell viability (d) under A/R injury, and this effect was silenced by AD14-3-3η RNAi. Values are presented as the mean ± SEM for five individual experiments. (A) P < 0.01 versus control group; (B) P < 0.01 versus A/R group; (C) P < 0.01 versus TSN + A/R group; (D) P < 0.05 versus A/R group; (E) P < 0.05 versus AD14-3-3ηRNAi group; (F) P < 0.01 versus AD14-3-3ηRNAi group.