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Antioxidant and antiapoptotic activities of idoxifene and estradiol in hepatic fibrosis in rats

机译：伊多昔芬和雌二醇对大鼠肝纤维化的抗氧化和抗凋亡活性

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Oxidative stress plays a causative role in the development of hepatic fibrosis and apoptosis. Estradiol (E2) is an antioxidant, and idoxifene is a tissue-specific selective estrogen receptor modulator. We have previously demonstrated that E2 inhibits hepatic fibrosis in a rat model of hepatic fibrosis induced with dimethylnitrosamine (DMN), and suppresses activation of the nuclear factor (NF)-kappaB proinflammatory transcription factor in cultured rat hepatocytes undergoing oxidative stress. This study reports on the antioxidant and antiapoptotic role of idoxifene and E2 in the DMN model of hepatic fibrosis. The DMN model rats were administered with idoxifene or E2, and were examined activity of superoxide dismutase (SOD) and glutathione peroxidase (GPx) and expression of Bcl-2 family proteins in the liver. During the course of hepatofibrogenesis after DMN treatment, serum levels of lactate dehydrogenase (LDH), a biomarker for necrosis, and hepatic levels of malondialdehyde (MDA), an end product of lipid peroxidation, increased rapidly for 3 days. On day 14, serum LDH levels normalized, and hepatic fibrosis developed with increased levels of MDA and collagen and decreased production of SOD and GPx in the liver. Fibrotic liver also showed downregulation of Bcl-2 and Bcl-x(L) expression and upregulation of Bad expression. Idoxifene and E2 suppressed DMN-mediated necrosis, lipid peroxidation, the loss of antioxidant enzyme activity, and proapoptotic status in Bcl-2 family protein expression as well as hepatic fibrosis. These findings indicate that, in addition to their antiinflammatory and antifibrotic action, idoxifene and E2 could enhance antioxidant and antiapoptotic activity in hepatic fibrosis in rats. (C) 2003 Elsevier Inc. All rights reserved. [References: 30]
机译：氧化应激在肝纤维化和细胞凋亡的发展中起重要作用。雌二醇（E2）是抗氧化剂，而伊多昔芬是组织特异性选择性雌激素受体调节剂。先前我们已经证明，E2在由二甲基亚硝胺（DMN）诱导的肝纤维化大鼠模型中抑制肝纤维化，并在经历氧化应激的培养大鼠肝细胞中抑制核因子（NF）-kappaB促炎转录因子的激活。这项研究报道了在肝纤维化DMN模型中，伊多昔芬和E2的抗氧化和抗凋亡作用。给DMN模型大鼠施用伊多昔芬或E2，并检查其超氧化物歧化酶（SOD）和谷胱甘肽过氧化物酶（GPx）的活性以及肝脏中Bcl-2家族蛋白的表达。在DMN处理后的肝纤维化过程中，血脂坏死的生物标志物乳酸脱氢酶（LDH）的血清水平和脂质过氧化作用的终产物丙二醛（MDA）的肝水平迅速升高了3天。在第14天，血清LDH水平恢复正常，肝纤维化随着MDA和胶原蛋白水平的增加以及肝脏中SOD和GPx产量的降低而发展。肝纤维化还显示出Bcl-2和Bcl-x（L）表达下调和Bad表达上调。艾多昔芬和E2抑制DMN介导的坏死，脂质过氧化，抗氧化酶活性的丧失以及Bcl-2家族蛋白表达以及肝纤维化中的凋亡状态。这些发现表明，除了抗炎和抗纤维化作用外，伊多昔芬和E2还可以增强大鼠肝纤维化的抗氧化和抗凋亡活性。 （C）2003 Elsevier Inc.保留所有权利。 [参考：30]

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