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首页> 外文期刊>American Journal of Physiology >Upregulation of endothelial nitric oxide synthase in rat aorta after ingestion of fish oil-rich diet.
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Upregulation of endothelial nitric oxide synthase in rat aorta after ingestion of fish oil-rich diet.

机译：摄入富含鱼油的饮食后大鼠主动脉内皮一氧化氮合酶的上调。

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A previous study with aortic segments isolated from rats fed a fish oil-rich diet indicated an increase in acetylcholine-induced nitric oxide (.NO)-mediated relaxation. However, it remained to be elucidated whether a fish oil-rich diet affects the vascular activity per se and the point of the.NO-cGMP pathway at which fish oil acts. For this purpose, two groups of Sprague-Dawley rats were fed a semipurified diet containing 5% lipids, either corn oil (CO) or menhaden oil (MO), for 8 wk. We studied the mRNA and protein levels of endothelial NO synthase (eNOS) and NOS activity. The bioavailability of vascular.NO was assessed directly by electron spin resonance spectroscopy. The levels of cGMP, l-arginine, and l-citrulline were also evaluated in homogenates. Superoxide anion (O(2)(-).) production and related antioxidant activities were also studied in aortic segments. The aortic content of eNOS mRNA was increased in rats fed the MO-rich diet. This resulted in increases in both eNOS protein levels (70% relative to the rats fed the CO-rich diet) and NOS activity (102%);.NO production increased by 90%, cGMP levels increased by 100%, and l-arginine decreased by 30%. No change in aortic O(2)(-). production was caused by dietary MO. The upregulation of the eNOS-cGMP pathway induced by dietary MO may contribute to the maintenance of vascular homeostasis and explain its beneficial effect in the prevention of arterial diseases.
机译：先前对从富含鱼油的大鼠中分离出的主动脉段进行的研究表明，乙酰胆碱诱导的一氧化氮（.NO）介导的舒张作用增加。但是，尚需阐明富含鱼油的饮食是否会影响血管活性本身以及鱼油起作用的NO-cGMP途径。为此，向两组Sprague-Dawley大鼠喂食半精制饮食，其中含有5％的脂质（玉米油（CO）或薄荷油（MO）），持续8周。我们研究了内皮NO合酶（eNOS）和NOS活性的mRNA和蛋白水平。血管NO的生物利用度通过电子自旋共振光谱直接评估。还对匀浆中的cGMP，1-精氨酸和1-瓜氨酸的水平进行了评估。还研究了主动脉段中的超氧阴离子（O（2）（-）。）生产和相关的抗氧化活性。喂食富含MO的大鼠的eNOS mRNA主动脉含量增加。这导致eNOS蛋白水平（相对于喂食富含CO的饮食的大鼠而言为70％）和NOS活性（102％）均增加; NO产量增加90％，cGMP水平增加100％，L-精氨酸增加下降了30％。主动脉O（2）（-）没有变化。生产是由饮食MO引起的。饮食MO诱导的eNOS-cGMP途径的上调可能有助于维持血管稳态，并解释其在预防动脉疾病中的有益作用。

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