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首页> 外文期刊>Life sciences >Therapeutic effect of glycyrrhetinic acid in MRL lpr/lpr mice: implications of alteration of corticosteroid metabolism.
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Therapeutic effect of glycyrrhetinic acid in MRL lpr/lpr mice: implications of alteration of corticosteroid metabolism.

机译：甘草次酸对MRL lpr / lpr小鼠的治疗作用：皮质类固醇代谢改变的意义。

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Glycyrrhetinic acid (GA) inhibits 11beta-hydroxysteroid dehydrogenase and increases the levels and thus the action of endogenous glucocorticoid. We considered that GA could be used effectively for treatment of autoimmune diseases that have been treated by synthetic glucocorticoids. In this report, we demonstrated that GA delayed the development of autoimmune disease in spontaneously autoimmune strain MRL lpr/lpr (referred to as lpr) mice. GA was administered via drinking water at approximately 5 mg/kg/day for 170 days. An increase of urine protein levels in the mice treated with GA was delayed as compared to the control mice. After GA treatment began, urinary protein levels in the GA-treated mice were found to be significantly lower than vehicle-treated mice (p<0.05) between days 18 to 50. At 3 weeks of GA treatment serum IgG levels were lowered significantly in comparison with the control mice (p<0.03). In this circumstance, 11beta-HSD activities in liver and kidney were significantly inhibited by GA treatment (p<0.03, p<0.04 respectively). Concentration of corticosterone and dehydrocorticosterone in liver significantly increased after 3 weeks of GA treatment (p<0.02, p<0.01 respectively). In contrast to the local tissue levels of corticosteroids, the serum concentration of dehydrocorticosterone significantly decreased with GA treatment (p<0.02). These data suggest that GA could modify the local and systemic homeostasis of steroid metabolism in lpr mice. We concluded that the continuous treatment of GA is able to retard the development of autoimmune disease by suppressing urinary protein excretion and serum IgG levels in lpr mice. Modulation of local tissue levels as well as serum levels of corticosteroid by GA may thus be implicated in the therapeutic efficacy of GA.
机译：甘草次酸（GA）抑制11β-羟类固醇脱氢酶并增加其含量，从而增加内源性糖皮质激素的作用。我们认为GA可以有效地用于治疗已由合成糖皮质激素治疗的自身免疫性疾病。在此报告中，我们证明了GA会延迟自发性自身免疫株MRL lpr / lpr（称为lpr）小鼠的自身免疫疾病的发展。通过饮用水以每天约5 mg / kg的剂量施用GA，持续170天。与对照小鼠相比，用GA治疗的小鼠尿蛋白水平的升高被延迟。开始GA治疗后，发现GA治疗小鼠中的尿蛋白水平显着低于媒介物治疗小鼠（p <0.05）（第18天至第50天之间）。在GA治疗3周后，血清IgG水平显着降低。用对照小鼠（p ＜0.03）。在这种情况下，GA治疗显着抑制了肝脏和肾脏中11beta-HSD的活性（分别为p <0.03，p <0.04）。 GA治疗3周后，肝脏中皮质酮和脱氢皮质酮的浓度显着增加（分别为p <0.02，p <0.01）。与局部皮质类固醇激素水平相比，GA治疗后血清脱氢皮质酮水平显着降低（p <0.02）。这些数据表明，GA可以改变lpr小鼠类固醇代谢的局部和全身稳态。我们得出的结论是，GA的连续治疗能够通过抑制lpr小鼠的尿蛋白排泄和血清IgG水平来延迟自身免疫疾病的发展。 GA对局部组织水平以及皮质类固醇的血清水平的调节因此可能与GA的治疗功效有关。

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