摘要
目的:观察丙泊酚对大鼠肝脏缺血再灌注后细胞凋亡及半胱天冬蛋白酶3(caspase3)的表达的影响,探讨丙泊酚的肝脏保护作用及其可能机制。方法:成年封闭群SD雄性大鼠56只,随机分为:Sham组;IR2组;IR6组;IR24组;P2组;P6组;P24组。P组自缺血前30 min静脉输注丙泊酚1 mg.kg-1.min-1,Sham组及IR组按0.1 mL.kg-1.min-1速率输注乳酸钠林格氏液,时间30 min。在相应的时间点处死动物,检测肝脏病理、细胞凋亡(TUNEL)、caspase3的表达及超氧化物歧化酶(SOD)和丙二醛(MDA)水平。结果:IR组再灌注后AI值(Apoptosis Index)及caspase3表达较sham组及P组明显增加,以再灌注后6 h最为明显。IR组SOD水平明显低于P组而MDA水平明显高于P组。结论:肝脏I/R后,Caspase3活性片段表达增加,肝细胞凋亡数目增加;丙泊酚通过抑制氧自由基的作用、下调caspase3的活性等机制,减少肝细胞的凋亡,减轻肝脏I/R损伤。
Objective: To observe the changes in caspase3 expression and apoptosis after liver ischemia/ reperfusion (I/R) , and to clarify whether propofol has a liver protection effect and the possible mechanism. Methods: Male SD rats (n =56) were randomly divided into 7 groups. Propofol was infused at 1 mg·kg^-1·min^-1 for 30 min before ischemia, and the same volume of sodium lactate/Ringer's solution was infused for 30 min in sham and I/R control groups. Apoptosis (TUNEL) , SOD, MDA and caspase3 expression were detected at the points of 2, 6 and 24 h after reperfusion. Results: Apoptosis index (AI) was greatly increased after reperfusion in ischemic groups ; propofol significantly reduced AI after ischemia (P 〈 0.05). Little caspase3 was expressed in sham group, but the expression was greatly increased in I/R groups. The expressions in propofol groups were also increased, but significantly lower than I/R control groups (P 〈 0.05). SOD levels were decreased in propofol groups, but were higher than in I/R control groups. MDA levels in propofol groups were lower than those in I/R control groups. Conclusion: Caspase3 expression and AI are greatly increased after liver I/R injury. Propofol can decrease caspase3 expression and liver cell apoptosis, suggesting a liver protection effect.
出处
《中国新药杂志》
CAS
CSCD
北大核心
2009年第11期1038-1041,共4页
Chinese Journal of New Drugs