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目的 :探讨线粒体PLA2 (MitochondrialPLA2 ,mtPLA2 )在严重烧伤早期心肌线粒体损害中的作用。方法 :取正常及伤后 1、3、6、12、2 4h大鼠心肌分离线粒体 ,测其呼吸功能及Ca2 + 浓度 ( [Ca2 + ] m)、mtPLA2活性。结果 :①心肌线粒体呼吸控制率 (RCR )伤后 1h升高 ,3、6、12、2 4h明显低于正常组 ,Ⅲ态呼吸速率(ST3 )变化与RCR平行 ,ST4 仅于伤后 3h有明显升高 ;②伤后各时相点 [Ca2 + ] m 均明显升高 ,而mtPLA2 活性于伤后 3、6、12、2 4h显著高于正常组 ;③伤后 3、6hRCR与mtPLA2 活性呈明显负相关 (r =-0 683 5 ,P <0 0 1;r =-0 5 419,P <0 0 1)。结论 :伤后 [Ca2 + ] m 升高可激活mtPLA2 ,后者在严重烧伤早期心肌线粒体损害中起重要作用。
Objective: To investigate the role of Mitochondrial PLA2 (mtPLA2) in mitochondrial damage during early stage of severe burn. Methods: Mitochondria were isolated from normal and post-injury 1,3,6,12,24 h rat myocardium and their respiratory function and Ca2 + concentration ([Ca2 +] m) and mtPLA2 activity were measured. Results: (1) Myocardial mitochondrial respiratory control rate (RCR) increased 1 hour after injury, 3,6,12,24h was significantly lower than the normal group, Ⅲ state respiration rate (ST3) changes parallel with RCR, ST4 only 3h after injury (2) The levels of [Ca2 +] m were significantly increased at various time points after injury, while the activity of mtPLA2 at 3, 6, 12 and 24 hours after injury was significantly higher than that of normal group. ③Rats and mtPLA2 activities (R = -0 683 5, P <0.01; r = -0 5 419, P <0.01). CONCLUSION: Increased [Ca2 +] m activates mtPLA2 after injury, which plays an important role in myocardial mitochondrial damage during severe burn injury.