失血性休克-复苏损伤降低小鼠骨骼肌脂肪氧化能力及过氧化物酶激活受体的表达

Hemorrhagic shock-resuscitation injury decreases fatty acid oxidation and peroxisome proliferator-activated receptor in the skeletal muscle

目的:研究小鼠失血性休克-复苏损伤后骨骼肌脂质氧化及过氧化物酶激活受体表达的变化。方法:将48只小鼠分成六组,即假手术对照组(Sham组)及按小鼠控制性失血休克-复苏损伤后处死时间的不同分为第1天(D1)组、第2天(D2)组、第3天(D3)组、第4天(D4)组和第5天(D5)组。取小鼠比目鱼肌组织,检测脂质氧化相关蛋白及其基因的表达水平。结果:造模后小鼠骨骼肌组织中的肉碱棕榈酸转移酶-1(CPT-1b)、脂肪酸转运蛋白1(FATP-1)、过氧化物酶激活受体(PPAR-α)和PPAR-β蛋白及基因表达水平明显降低。结论:失血休克-复苏后小鼠调节脂质氧化的核受体表达下降,脂肪氧化能力受损。

Objective： The study was designed to study the influence of hemorrhagic shock-resuscitation injury on mice fatty acid oxidation and peroxisome proliferator-activated receptor expression. Methods： 48 C57 BL /6 mice were assigned to 6groups. One was sham group without any surgery. According to the different time when the mice were sacrificed after hemorrhagic shock-resuscitation injury,the other 5groups were defined as Day 1 postoperative group（ D1 group）,Day 2 postoperative group（ D2 group）,Day 3 postoperative group（ D3 group）,Day4 postoperative group（ D4 group） and Day 5 postoperative group（ D5 group）. Soleus tissue were collected for the protein and gene expression related to fatty acid oxidation. Results： After hemorrhagic shock-resuscitation injury,the protein and gene expression of CPT-1b,FATP-1,PPAR-αand PPAR-β in muscle tissue decreased significantly.Conclusion： Hemorrhagic shock-resuscitation injury may decrease the nuclear hormone receptors in muscle which regulate the lipid metabolism and impair the fat β-oxidation.