CAJ | 학술논문

目的:观察17β-雌二醇替代治疗对卵巢切除大鼠心肌组织中一氧化氮(NO)和内皮源性一氧化氮合酶(eNOS)的影响.方法:成年雌性SD大鼠经双侧卵巢切除术,假手术组作为对照,术后3周随机分为假手术组,模型对照组,17β-雌二醇(0.1mg·kg-1·d-1)和溶媒(芝麻油)皮下注射治疗组,处理6周,记录大鼠的血压、心率、子宫重量;检测血中雌二醇的含量;亚硝酸还原酶法检测心肌匀浆中NO含量;Westem b1ot分析心肌中eNOS及eNOS调节蛋白小凹蛋白-1(caveolin-1)的蛋白表达情况.结果:17β-雌二醇治疗组的心率(314±16次/分)较其他各组低,与溶媒对照组比较,雌二醇替代治疗组心肌匀浆中NO的含量增加一倍,eNOS蛋白表达明显增加(P＜0.01),而作为eN0S的内源性抑制物caveolin-1的表达却明显减少(P＜0.05).结论:雌激素替代治疗直接增加卵巢切除大鼠心肌eNOS的表达量以及NO的产生,减少抑制eNOS活性的小凹蛋白1表达.
목적:관찰17β-자이순체대치료대란소절제대서심기조직중일양화담(NO)화내피원성일양화담합매(eNOS)적영향.방법:성년자성SD대서경쌍측란소절제술,가수술조작위대조,술후3주수궤분위가수술조,모형대조조,17β-자이순(0.1mg·kg-1·d-1)화용매(지마유)피하주사치료조,처리6주,기록대서적혈압、심솔、자궁중량;검측혈중자이순적함량;아초산환원매법검측심기균장중NO함량;Westem b1ot분석심기중eNOS급eNOS조절단백소요단백-1(caveolin-1)적단백표체정황.결과:17β-자이순치료조적심솔(314±16차/분)교기타각조저,여용매대조조비교,자이순체대치료조심기균장중NO적함량증가일배,eNOS단백표체명현증가(P＜0.01),이작위eN0S적내원성억제물caveolin-1적표체각명현감소(P＜0.05).결론:자격소체대치료직접증가란소절제대서심기eNOS적표체량이급NO적산생,감소억제eNOS활성적소요단백1표체.
To investigate whether 17β-estradiol influences the production of nitric oxide (NO) and expression of eNOS in ovariectomized (OVX) rats heart.METHODS: Female mature SpragueDawley rats were subjected to a bilateral ovariectomy, and sham operation as control. OVX rats were randomly assigned to the following treatments: 17β-estradiol (100 μgkg-1 in 100 μl sesame oil sc daily), 17β-estradiol vehicle ( 100 μl sesame oil sc daily) and OVX control. The treatment lasted 6 weeks. Blood pressure, heart rate, plasma estradiol,uterine weights and nitrite production in the myocardium were studied. Western blot analysis was used to assay the protein expression of eNOS and caveolin-1. RESULTS:The heat rates in 17β-estradiol treatment group (314 + 16 ＜ 0.05). Compared with vehicle group, nitrite production increased one fold in the hearts of E2 treatment group, the abundance of eNOS protein showed a significant increase (P ＜ 0.01). Concurrently caveolin-1 protein, an endogenous eNOS inhibitor, protein expression abundance was significantly decreased ( P ＜ 0.05) in the E2 supplement group. CONCLUSION: Estrogen supplementation directly increases eNOS functional activity and NO production in rat heart, this effect may be related to estrogen-indueed deceasing of heart rates.