摘要
目的观察束缚应激对雄性Wistar大鼠心肌过氧化体增殖物激活型受体α(PPARα)、PPARβ和肌型肉碱棕榈酰转移酶-I(M-CPT-I)mRNA表达的影响。方法健康雄性Wistar大鼠,采用束缚应激模型,实验组大鼠每天给予束缚应激2次,每次3h。按照有无应激和应激时间长短分为正常对照组(C)、束缚1w(R1)、束缚2w(R2)和束缚4w组(R4)。采用逆转录酶多聚酶链反应(RT-PCR)检测各组心肌PPARα、PPARβ和M-CPT-I的mRNA表达水平。结果束缚应激1、2、4w大鼠心肌PPARαmRNA和M-CPT-I mRNA水平较正常对照组明显升高(P<0.01或P<0.05);心肌PPARβmRNA水平较正常对照组变化不明显(P>0.05)。结论束缚应激上调心肌PPARα和M-CPT-I mRNA表达,对PPARβ无明显影响,PPARα可能促进束缚应激大鼠脂肪酸氧化增加。
Objective To explore the effects of restraint stress on the expressions of peroxisome proliferator - activated receptor - α （ PPARα ）, peroxisome proliferator - activated receptor - β （ PPARβ ） and muscle carnitine palmitoyl transferase - I （ M - CPT - I） mRNA in the myocardium of rat. Methods According to the duration of restraint stress,healthy Wistar rats were divided into four groups ： control group （ no restraint）, R1 group （ 1 - week restraint）, R2 group （2 -week restraint） and R4 group（4 - week restraint）. In three experimental groups, animals were under restraint stress twice a day and 3 hours per stress. After the the restraint stress experiment ended,the expressions of PPARα,PPARβ and M - CPT - I mRNA in the myocardium were evaluated by reverse transcription polymerase chain reaction（ RT - PCR）. Results The expressions of myocardial PPARα mRNA and M - CPT - I mRNA in three groups under restraint stress were all significantly higher than those in control group （ P 〈 0.01 or P 〈 0.05 ）, while the expression of PPARβ mRNA had no significant change compared with control group（ P 〉 0.05 ）. Conclusion Restraint stress can up - regulate the expressions of PPARα and M - CPT - I mRNA, but it had no effect on the expression of PPARβ mRNA. PPARoL may increase the myocardial fatty oxidation in rats under restraint stress. [
出处
《西南国防医药》
CAS
2010年第1期10-12,共3页
Medical Journal of National Defending Forces in Southwest China
关键词
束缚应激
心肌
过氧化体增殖物激活型受体Α
过氧化体增殖物激活型受体β
肌型肉碱棕榈酰转移酶-I
restraint stress
myocardium
peroxisome proliferator - activated receptor - α
peroxisome proliferator - activated receptor - β
muscle carnitine palmitoyl transferase - I
