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首页> 外文期刊>Cell biology international. >17‐β estradiol attenuates the pro‐oxidant activity of corticotropin‐releasing hormone in macroendothelial cells
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17‐β estradiol attenuates the pro‐oxidant activity of corticotropin‐releasing hormone in macroendothelial cells

机译：17-β雌二醇衰减在宏观中细胞中释放皮质激素释放激素的促氧化活性

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Abstract Corticotropin‐releasing hormone, which is the predominant regulator of neuroendocrine responses to stress, attenuates inflammation through stimulation of glucocorticoid release. Enhanced corticotropin‐releasing hormone expression has been detected in inflammatory cells of the vascular endothelium, where it acts as a local regulator of endothelial redox homeostasis. Estrogens have beneficial effects on endothelial integrity and function, though the mechanism underlying their antioxidative effect remains as yet largely unknown. We therefore investigated the effect of 17β‐estradiol on pro‐oxidant action of corticotropin‐releasing hormone in vitro in macroendothelial cells, and, more specifically, the role of 17β‐estradiol on corticotropin‐releasing hormone‐induced activities/release of the antioxidant enzymes namely, endothelial nitric oxide synthase, superoxide dismutase, catalase, and glutathione. We observed that 17β‐estradiol abolished the stimulatory effect of corticotropin‐releasing hormone on intracellular reactive oxygen species levels and counteracted its inhibitory effect on endothelial nitric oxide synthase activity and nitric oxide release. In addition, 17β‐estradiol significantly induced superoxide dismutase and catalase activity, an effect that was not significantly influenced by corticotropin‐releasing hormone. Finally, 17β‐estradiol significantly increased glutathione levels and the glutathione/glutathione?+?glutathione disulfide ratio, an action that was partially blocked by corticotropin‐releasing hormone. Our results reveal that 17β‐estradiol counterbalances corticotropin‐releasing hormone‐mediated pro‐inflammatory action and thereby maintains the physiological threshold of the endothelial cell redox environment. These observations may be of importance, considering the protective role of estrogen in the development of atherosclerosis.
机译：摘要皮质皮蛋白 - 释放激素，即神经内分泌反应对应激的主要调节剂，通过刺激糖皮质激素释放来衰减炎症。在血管内皮的炎性细胞中检测到增强的皮质大发释放激素表达，其中它充当内皮氧化还原稳态的局部调节剂。雌激素对内皮完整性和功能有益的影响，尽管其抗氧化效应的机制仍然很大程度上尚不清楚。因此，我们研究了17β-estradiol对甲状腺细胞体外体外皮里罗呤 - 释放激素的促氧化作用的影响，更具体地，17β-雌二醇对皮质甾醇释放激素诱导的活性/脱氧剂酶释放的作用即，内皮一氧化氮合酶，超氧化物歧化酶，过氧化氢酶和谷胱甘肽。我们观察到，17β-雌二醇废除了皮质甾醇释放激素对细胞内反应性氧物质水平的刺激作用，并抵消了其对内皮内氧化氮合酶活性和一氧化氮释放的抑制作用。此外，17β-雌二醇显着诱导超氧化物歧化酶和过氧化氢酶活性，其效果不会受到皮质甾醇释放激素的显着影响。最后，17β-雌二醇显着增加了谷胱甘肽水平和谷胱甘肽/谷胱甘肽α+？谷胱甘肽二硫化物比例，其由皮质甾醇释放激素部分阻断的作用。我们的研究结果表明，17β-雌二醇平衡皮质甾醇释放激素介导的促炎作用，从而保持内皮细胞氧化还原环境的生理阈值。考虑到雌激素在动脉粥样硬化发展中的保护作用，这些观察可能具有重要性。

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