束缚应激对大鼠血脂及肝脏PPARα、L-CPT-ⅠmRNA和蛋白表达的影响

EFFECT OF RESTRAINT STRESS ON BLOOD LIPID AND EXPRESSIONS OF LIVER PPARα,L-CPT-Ⅰ mRNA & PROTEIN IN RATS

目的观察束缚应激后大鼠血脂和肝脏过氧化酶体增殖物激活型受体(PPARα)、肝型肉碱棕榈酰转移酶-Ⅰ(L-CPT-Ⅰ)mRNA和蛋白的变化,初步探讨应激与血脂的关系。方法健康雄性Wistar大鼠,分为正常对照组(C)、束缚1周组(R1)、束缚2周组(R2)和束缚4周组(R4),每组8只。全自动生化仪测定血脂水平,铜显色法测定血清中游离脂肪酸(FFA)水平。分别用RT-PCR和Western Blot方法检测肝脏PPARα及其靶基因L-CPT-ⅠmRNA和蛋白表达水平。结果束缚应激组皮质醇和去甲基肾上腺素水平均明显高于对照组(P<0.01)。R1、R2、R4组大鼠血清FFA分别为(836.33±90.32)、(795.01±62.12)、(829.56±72.64)μmol/L,均明显高于C组〔(620.83±52.21)μmol/L,P<0.01〕。同样,R1、R2、R4组大鼠血清TG和HDL-C均明显高于C组(P<0.05,P<0.01)。与C组相比,R1、R2、R4组大鼠肝脏中PPARα和L-CPT-ⅠmRNA和蛋白表达均增加(P<0.01)。各应激组间这些指标变化差异均无显著性(P>0.05)。结论束缚应激后大鼠血清FFA、TG和HDL-C水平升高,这可能与其肝脏PPARα及L-CPT-Ⅰ表达增加有关。

Objective To observe the effect of restraint stress on blood lipid and the expressions of liver peroxisome proliferator-activated receptor α（PPARα）,liver carnitine palmitoyl transferase-Ⅰ（L-CPT-Ⅰ）mRNA protein in rat,in order to explore the relationship between stress and blood lipid. Methods Thirty-two Wistar rats were divided into four groups： control,and rats under 1 week（R1）,2 weeks（R2）,and 4 weeks（R4） of restraint stress. The level of triglyceride（TG）,total cholesterol（TC） and free fatty acids（FFA） was detected. The expression of PPARα and L-CPT-ⅠmRNA protein in the liver was evaluated by RT-PCR and Western blot. Results The level of serum cortisol and noradrenaline in3 restraint stress groups was significantly higher than in control group（P〈0. 01）. The level of serum FFA in R1,R2,R4,restraint stress groups〔（836. 33 ±90. 32）,（795. 01 ± 62. 12）,（829. 56 ± 72. 64）μmol /L respectively〕was higher than in control group〔（620. 83 ±52. 21）μmol /L,P〈0. 05〕. Similarly,the level of serum TG,HDL-C,as well as the expression of PPARα and L-CPT-ⅠmRNA protein in 3 restraint groups were all higher than in control group（P〈0. 05,P〈0. 01）.However,there was no significant difference in these indicators among 3 restraint stress groups（p〉0. 05）. Conclusion The level of serum FFA,TG,and HDL-C in restraint stressed rats was increased,which may be related to the upregulation of liver PPARα and L-CPT-Ⅰ.