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17β-雌二醇增加卵巢切除大鼠心肌内皮型一氧化氮合酶的表达和一氧化氮生成
引用本文:汤勇波,王乾蕾,朱炳阳,黄红林,廖端芳.17β-雌二醇增加卵巢切除大鼠心肌内皮型一氧化氮合酶的表达和一氧化氮生成[J].中国临床药理学与治疗学,2004,9(4):411-416.
作者姓名:汤勇波  王乾蕾  朱炳阳  黄红林  廖端芳
作者单位:南华大学药物药理研究所,衡阳,421001,湖南
基金项目:ThisworkwaskindlysupportedbytheHunanProvincialBureauofHealthTraditionalDrugFoundation(№ 2 0 2 0 72 )
摘    要: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 ;Westernblot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 .0 1) ,而作为eNOS的内源性抑制物caveolin 1的表达却明显减少 (P <0 .0 5 )。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。

关 键 词:17β-雌二醇  一氧化氮  内皮型一氧化氮合酶  小凹蛋白

Study of 17β-Estradiol supplementation on increasing eNOS expression and NO production in ovariectomized rat heart
Abstract.Study of 17β-Estradiol supplementation on increasing eNOS expression and NO production in ovariectomized rat heart[J].Chinese Journal of Clinical Pharmacology and Therapeutics,2004,9(4):411-416.
Authors:Abstract
Abstract: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.
Keywords:estradiol  nitric oxide  endothelial nitric oxide synthase  caveolin
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