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

Inhibition of RASD1 facilitates the therapeutic effects of Sevoflurane on I/R injury in mice after TKA by activating the PKA pathway. (A) diagram indicating the different treatment protocols in mice. I/R mice were treated with Sevoflurane + sh-RASD1, Sevoflurane + sh-NC, Sevoflurane + veh and Sevoflurane + H89. (B) Western blot analysis of RASD1, cAMP, PKA, CREB, pro-caspase-3, PCNA, Bcl-2, Bax and cleaved caspase-3 levels and the extents of PKA and CREB phosphorylation in synovial tissues. (C) Cell apoptosis measured by TUNEL assay (× 200). (D) HE staining of the synovial tissues (× 200). (E), Levels of IFN-γ, IL-6 and TNF-α in serum of mice measured by ELISA. * p p t-test. n = 10.

Figure 5. Inhibition of RASD1 facilitates the therapeutic effects of Sevoflurane on I/R injury in mice after TKA by activating the PKA pathway. (A) diagram indicating the different treatment protocols in mice. I/R mice were treated with Sevoflurane + sh-RASD1, Sevoflurane + sh-NC, Sevoflurane + veh and Sevoflurane + H89. (B) Western blot analysis of RASD1, cAMP, PKA, CREB, pro-caspase-3, PCNA, Bcl-2, Bax and cleaved caspase-3 levels and the extents of PKA and CREB phosphorylation in synovial tissues. (C) Cell apoptosis measured by TUNEL assay (× 200). (D) HE staining of the synovial tissues (× 200). (E), Levels of IFN-γ, IL-6 and TNF-α in serum of mice measured by ELISA. * p < 0.05 vs. I/R mice treated with Sevoflurane + sh-NC; # p < 0.05 vs. I/R mice treated with Sevoflurane + veh. The above data were all measurement data and expressed as mean ± standard deviation. Data between two groups were analyzed using t-test. n = 10.