CAJ | 학술논문

目的观察疲劳与束缚应激对大鼠主动脉血管内皮功能与肉碱棕榈酰转移酶-Ⅰ(CPT-Ⅰ)、过氧化物酶体增殖物激活受体δ(PPARδ)、5-羟色氨1D(5-HT1D)、5-羟色氨2A(5-HT2A)受体表达的影响.方法健康雄性Wisar大鼠45只,随机分为对照组、疲劳组和束缚组.观察大鼠一般状况、主动脉内皮细胞形态和结构,检测血中内皮素(ET-1)和一氧化氮(NO)水平,采用实时PCR和Western印迹检测主动脉CPT-Ⅰ、PPARδ和5-HT1D、5-HT2A受体基因和蛋白表达.结果与对照组比较,疲劳和束缚应激均可导致大鼠主动脉内皮结构损伤,血清ET-1水平升高[(124±18)ng/L比(161±18)ng/L、(154±17)ng/L](P＜0.01,P＜0.05),血浆NO水平降低[(63±16)μmol/L比(39±8)μmol/L、(41±7)μmol/L](P＜0.05);疲劳应激大鼠主动脉CPT-Ⅰ和PPAR-δmRNA表达下调,分别为[(1.23±0.21)比(0.42±0.05)]、[(1.09±0.10)比(0.25±0.07)](均P＜0.01),同时CPT-Ⅰ和PPAR-δm蛋白表达亦下调[(1.32±0.07)比(0.83±0.04)]、[(1.41±0.05)比(0.75±0.06)](均P＜0.01);疲劳、束缚应激均可导致主动脉5-HT1D受体mRNA和蛋白表达下调[(1.10±0.15)比(0.46±0.13)、(0.45±0.02)],[(1.19±0.05)比(0.71±0.06)、(0.70±0.05)](P＜0.01);同时5-HT2A受体mRNA和蛋白表达上调[(0.99±0.08)比(6.73±0.46)、(7.01±1.56)],[(0.64±0.03)比(0.79±0.05)、(0.82±0.03)](均P＜0.01).结论过度疲劳与情绪抑郁均可损伤血管内皮结构与功能,其中肉碱代谢异常为主的能量变化和5-HT受体调节异常在其中发挥重要作用.
목적 관찰피로여속박응격대대서주동맥혈관내피공능여육감종려선전이매-Ⅰ(CPT-Ⅰ)、과양화물매체증식물격활수체δ(PPARδ)、5-간색안1D(5-HT1D)、5-간색안2A(5-HT2A)수체표체적영향.방법 건강웅성Wisar대서45지,수궤분위대조조、피로조화속박조.관찰대서일반상황、주동맥내피세포형태화결구,검측혈중내피소(ET-1)화일양화담(NO)수평,채용실시PCR화Western인적검측주동맥CPT-Ⅰ、PPARδ화5-HT1D、5-HT2A수체기인화단백표체.결과 여대조조비교,피로화속박응격균가도치대서주동맥내피결구손상,혈청ET-1수평승고[(124±18)ng/L비(161±18)ng/L、(154±17)ng/L](P＜0.01,P＜0.05),혈장NO수평강저[(63±16)μmol/L비(39±8)μmol/L、(41±7)μmol/L](P＜0.05);피로응격대서주동맥CPT-Ⅰ화PPAR-δmRNA표체하조,분별위[(1.23±0.21)비(0.42±0.05)]、[(1.09±0.10)비(0.25±0.07)](균P＜0.01),동시CPT-Ⅰ화PPAR-δm단백표체역하조[(1.32±0.07)비(0.83±0.04)]、[(1.41±0.05)비(0.75±0.06)](균P＜0.01);피로、속박응격균가도치주동맥5-HT1D수체mRNA화단백표체하조[(1.10±0.15)비(0.46±0.13)、(0.45±0.02)],[(1.19±0.05)비(0.71±0.06)、(0.70±0.05)](P＜0.01);동시5-HT2A수체mRNA화단백표체상조[(0.99±0.08)비(6.73±0.46)、(7.01±1.56)],[(0.64±0.03)비(0.79±0.05)、(0.82±0.03)](균P＜0.01).결론 과도피로여정서억욱균가손상혈관내피결구여공능,기중육감대사이상위주적능량변화화5-HT수체조절이상재기중발휘중요작용.
Objective To investigate the effect of fatigue and restraint stress on the expressions of CPT (carnitine palmitoyltransferase )-Ⅰ , PPAR (peroxisome proliferator-activated receptor) δ, 5-HT (hydroxytryptamine) 1D and 5-HT2A receptors in aorta of rats. Methods A total of 45 healthy male Wistar rats were randomly divided into control group, excessive fatigue group and restraint stress group (n =15 each). The general condition, morphological changes of aortic endothelium cell and the blood levels of ET-1 (endothelin) and NO (nitric oxide ) were observed. The real-time reverse transcription PCR (polymerase chain reaction) and Western blot were used to detect the gene and protein expressions of CPT-Ⅰ , PPAR δ, 5-HT1D and 5-HT2A receptors in aorta. Results Compared with control group, the structural damages of endothelial cell were induced by excessive fatigue and restraint stress. The plasma levels of ET-1 increased [( 124 ± 18)ng/L vs( 161 ± 18 ) ng/L, ( 154 ± 17 ) ng/L] (P ＜ 0.01, P ＜ 0.05 )while the serum levels of NO decreased [(63 ± 16) μmol/L vs(39 ±8) μmol/L, (41 ±7) μmol/L] (P ＜0. 05); the mRNA expressions of CPT- Ⅰ and PPARδ decreased in excessive fatigue rats, [( 1.23 ± 0.21 )vs (0.42 ± 0.05 )], [( 1.09 ± 0.10) vs (0.25 ± 0.07 )] ( P ＜ 0.01 ); the protein expressions of CPT- Ⅰ and PPARδ decreased in excessive fatigue rats, [( 1.32 ± 0.07 ) vs (0. 83 ± 0.04 )], [( 1.41 ± 0.05 ) vs.(0.75 ± 0. 06)]; the mRNA and protein expressions of 5-HT1 D receptor decreased in excessive fatigue rats and restraint stress rats, [(1. 10 ±0.15)vs (0.46 ±0.13) ,(0.45 ±0.02)], [( 1. 19 ±0.05)vs (0.71±0. 06), (0.70 ±0.05 )] (P ＜ 0.01 ); the mRNA and protein expressions of 5-HT2A receptor increased in excessive fatigue rats and restraint stress rats, [(0.99 ± 0. 08 ) vs (6.73 ± 0.46 ), ( 7.01 ± 1.56 )],[(0.64±0. 03)vs (0. 79 ±0. 05), (0. 82 ±0. 03)] ( P ＜0. 01). Conclusion Excessive fatigue and restraint stress can injure the structure and function of endothelial cell. The changes in energy of abnormal carnitine metabolism and 5-HT receptors may play important roles.