Effect of dexmedetomidine on pulmonary microvascular endothelial cell injury induced by serum of mice with renal ischemia-reperfusion injury / 中华麻醉学杂志

ABSTRACT

Objective To evaluate the effect of dexmedetomidine on pulmonary microvascular en-dothelial cell(PMVEC)injury induced by the serum of mice with renal ischemia-reperfusion(I∕R)injury. Methods Renal I∕R was induced by clamping bilateral renal pedicles for 60 min followed by 24 h of reper-fusion. Primary PMVECs of mice were divided into 3 groups(n=20 each)using a random number tablecontrol group(group C), serum of mice underwent I∕R group(group I∕R)and dexmedetomidine group (group Dex). PMVECs were cultured with 10% serum of mice underwent sham operation in group C. PM-VECs were cultured with 10% serum of mice underwent I∕R injury in group I∕R. PMVECs were incubated for 3 h with dexmedetomidine at the final concentration of 0.1 μmol∕L before incubation with serum in group Dex. At 24 h of culture or incubation, the cell survival rate was detected by CCK8 assay, cell apoptosis by Hoechst 33258 staining, caspase-3 activity using colorimetric method, and the expression of Bcl-2 and Bax using Western blot. Results Compared with group C, the cell survival rate was significantly decreased, the apoptosis rate and activity of caspase-3 were increased, the expression of Bcl-2 was down-regulated, and the expression of Bax was up-regulated in I∕R and Dex groups(P<0.01). Compared with group I∕R, the cell survival rate was significantly increased, the apoptosis rate and activity of caspase-3 were de-creased, the expression of Bcl-2 was up-regulated, and the expression of Bax was down-regulated in group Dex(P<0.01). Conclusion Dexmedetomidine can reduce PMVEC injury induced by the serum of mice with renal I∕R injury, and the mechanism is related to regulating the expression of Bcl-2 and Bax and inhib-iting mitochondrial apoptosis pathway.