丙泊酚对过氧化氢诱导入脐静脉内皮细胞超氧化物歧化酶1表达的影响

Effects of propofol on expression of superoxide dismutase-1 in hydrogen dioxide mediated human umbilical vein endothelial cells

目的 探讨丙泊酚对过氧化氢（H2O2）诱导入脐静脉内皮细胞（human umbilical vein endothelial cells,HUVEC）超氧化物歧化酶1（superoxide dismutase-1,SOD1）表达的影响.方法 将体外培养24孔板中的HUVEC分为3部分：第1部分（分4组,每组6例）：①正常对照组（C组）;②H2O2刺激组（H组）：H2O2 200 μmol/L;③丙泊酚组（P组）：丙泊酚100μmol/L;④丙泊酚加H2O2刺激组（P＋H组）;第2部分（分5组,每组6例）：分别给予丙泊酚12.5、25、50、100、200 μmol/L预处理30 min后,再给予H2O2 200 μmol/L.第3部分（分5组,每组6例）：丙泊酚最佳浓度预处理30 min后,再给予H2O2 200μmol/L,分别培养6、12、24、36、48 h,采用Western blot观察HUVEC在H2O2刺激下,丙泊酚对HUVEC中SOD1表达影响的量效与时效关系.将96孔板中的HUVEC分为3组（每组5例）：①空白对照组（C组）;②H2O2刺激组（H组）;③丙泊酚＋H2O2组（P＋H组）,采用MTT法检测丙泊酚对HUVEC存活率的影响.结果 H2O2（200 μmol/L）刺激HUVEC后,能明显抑制HUVEC中SOD1的表达.丙泊酚预处理后,能部分逆转H2O2对HUVEC中SOD1的抑制作用.丙泊酚浓度为100μmol/L,H2O2刺激时间为24 h时,逆转效应达高峰.结论 丙泊酚可通过上调SOD1表达而减轻H2O2诱导HUVEC氧化应激损伤.

Objective To investigate the effects of propofol on the expression of superoxide dismutase-1 （SOD1 ） in hydrogen dioxide （H2O2）-mediated human umbilical vein endothelia cells （HUVEC）. Methods The HUVEC cultured in 24-well plate was with propofol 12.5, 25, 50, 100 and 200 μmol/L respectively for 30 min before H2O2 sitimulating HUVEC. Part 3 （divided into five groups, n=6）： the optimal concentration of propofol was used for pretreatment for 30 min before H2O2 sitimulated HUVEC,HUVEC was cultured for 6, 12, 24, 36 and 48 h accordingly. Western blot was used to determine the dose-depedent and time-dependent effect of propofol on the expression of SOD1 in HUVEC. The HUVEC which cultured in 96-well plate was divided into three groups assay was used to detect the survival rate of HUVEC. Results After the cells were pretreated with hydrogen peroxide （200 μmol/L）, the expression of SOD1 in HUVEC decreased dramatically,however, propofol can partially reverse this effect on H2O2 induced SOD1 expression. When HUVEC were pretr eated with 100 μmol/L propofol for 30 min before the treatment of H2O2, 24 h later, the expression of SOD1 reached to its highest level. Conclusion Propofol can protect endothelial cells from the injury of reactive oxygen species through up-regulating the expression of SOD1.