Research Paper Volume 13, Issue 9 pp 13333—13348

Figure 4. Sevoflurane treatment inhibits apoptosis and promotes proliferation in the skeletal muscle cells with I/R injury by inducing the RASD1-dependent PKA pathway activation. (A) Western blot analysis of cAMP, phosphorylated PKA and phosphorylated CREB levels in cells after treatment with HRO, Sevoflurane and RASD1 alteration/PKA pathway inhibition, * p < 0.05 vs. control cells; # p < 0.05 vs. HRO-treated cells; & p < 0.05 vs. cells treated with HRO + Sevoflurane + oe-NC; ! p < 0.05 vs. cells treated with HRO + Sevoflurane + sh-NC; @ p < 0.05 vs. cells treated with HRO + Sevoflurane + veh. (B) Western blot analysis of Bcl-2, PCNA, Bax, cleaved caspase-3 and pro-caspase-3 levels in cells after treatment with HRO, Sevoflurane and PKA pathway inhibition. (C) Cell proliferation after treatment with HRO, Sevoflurane and PKA pathway inhibition detected by EdU assay (× 200). (D) Cell apoptosis after treatment with HRO, Sevoflurane and PKA pathway inhibition measured by TUNEL assay (× 200). (E) Levels of IFN-γ, IL-6 and TNF-α in cell culture supernatant after treatment with HRO, Sevoflurane and PKA pathway inhibition measured by ELISA. In panel B-E, * p < 0.05 vs. cells treated with HRO + Sevoflurane + veh. The above data were all measurement data and expressed as mean ± standard deviation. Data among multiple groups were compared by one-way ANOVA, followed by Tukey’s multiple comparisons posttest. The experiment was repeated 3 times independently.