Research Paper Volume 13, Issue 9 pp 13333—13348

Sevoflurane protects against ischemia-reperfusion injury in mice after total knee arthroplasty via facilitating RASD1-mediated protein kinase A pathway activation

class="figure-viewer-img"

Figure 3. Sevoflurane treatment suppresses RASD1 expression to impede proliferation and stimulate apoptosis in skeletal muscle cells with I/R injury. (A) The expression pattern of RASD1 in cells after alteration of RASD1 detected using RT-qPCR. * p < 0.05 vs. the treatment with oe-NC (B) Protein level of RASD1 in cells after treatment with HRO, Sevoflurane and RASD1 alteration detected using Western blot analysis. * p < 0.05 vs. the treatment with oe-NC. # p < 0.05 vs. the treatment with sh-NC. Skeletal muscle cells were treated or not treated with HRO, HRO + Sevo, HRO + Sevoflurane +oe-NC, HRO + Sevoflurane + oe-RASD1, HRO + Sevoflurane + sh-NC and HRO + Sevoflurane + sh-RASD1. (C) Cell proliferation measured using EdU assay (× 200). (D) Cell apoptosis measured by TUNEL assay (× 200). (E) Western blot analysis of the RASD1 expression pattern in cells. (F) Levels of IFN-γ, IL-6 and TNF-α in cells measured by ELISA. * p < 0.05 vs. control cells; # p < 0.05 vs. HRO-treated skeletal muscle cells; & p < 0.05 vs. HRO cells treated with Sevoflurane and oe-NC; ! p < 0.05 vs. HRO cells treated with Sevoflurane and sh-NC. 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 cell experiment was repeated 3 times independently.