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硼抑制增殖细胞核抗原指数、含钼蛋白并改善肝癌中的氧化应激。

Boron inhibits the proliferating cell nuclear antigen index, molybdenum containing proteins and ameliorates oxidative stress in hepatocellular carcinoma.

机构信息

Department of Biochemistry, Faculty of Science, Jamia Hamdard, Hamdard Nagar, New Delhi 110062, India.

出版信息

Arch Biochem Biophys. 2013 Jan 15;529(2):66-74. doi: 10.1016/j.abb.2012.11.008. Epub 2012 Dec 3.

DOI:10.1016/j.abb.2012.11.008
PMID:23219601
Abstract

Hepatocellular carcinoma (HCC) is a common malignancy and the main cause of mortality in patients with chronic liver diseases. This study reports the inhibitory effect of boron on HCC induced in rats by administering thioacetamide (TAA) (0.03%) in drinking water for 400days. Boron (4mg/kg body weight) was administered orally after induction of carcinoma. Treatment was continued for 122days, and cell proliferation, histology and biochemistry of treated and control group of rats were studied. Proliferating cell nuclear antigen (PCNA), and [(3)H]-thymidine incorporation, which increased in rats exposed to carcinogen, significantly decreased after boron treatment. PCNA index decreased from 80 in HCC rats to 32 after boron treatment. In the control group, it was 20. Boron caused a dose-dependent decrease in carcinogen-induced [(3)H]-thymidine uptake by the rat hepatocyte. It could partially reverse the activity of selected biochemical indicators of hepatic damage, oxidative stress, selenium and serum retinol, which are depleted in liver cancer, and improved overall health of animal. The study implicates the elevated levels of mammalian molybdenum Fe-S containing flavin hydroxylases, which increase the free radical production and oxidative stress, consequently causing increased hepatic cell proliferation in HCC, and reports boron to ameliorate these changes in liver cancer.

摘要

肝细胞癌(HCC)是一种常见的恶性肿瘤,也是慢性肝病患者死亡的主要原因。本研究报告了硼对 TAA(0.03%)诱导的大鼠 HCC 的抑制作用,TAA 通过饮用水给予大鼠,持续 400 天。在诱导癌后,经口给予硼(4mg/kg 体重)。治疗持续 122 天,研究了硼处理和对照组大鼠的细胞增殖、组织学和生物化学。暴露于致癌剂的大鼠中增殖细胞核抗原(PCNA)和[(3)H]胸苷掺入增加,经硼处理后显著减少。PCNA 指数从 HCC 大鼠的 80 降至硼处理后的 32。在对照组中,它是 20。硼导致大鼠肝细胞中致癌剂诱导的[(3)H]胸苷摄取呈剂量依赖性下降。它可以部分逆转肝癌中肝脏损伤、氧化应激、硒和血清视黄醇等选定生化指标的活性,这些指标在肝癌中被耗尽,并改善动物的整体健康状况。研究表明,哺乳动物钼 Fe-S 含黄素羟化酶的水平升高,导致自由基产生和氧化应激增加,从而导致 HCC 中肝细胞增殖增加,并报告硼改善肝癌中的这些变化。

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