在小鼠诱导的肝细胞致癌过程中NOX4表达,氧化应激指数,PIIINP和肝组织病理学的顺序变化
Majid Jafari-Khorchani1, Kostas Pantopoulos2,3, Mohammad-Jalil Zare-Mehrjardi1
1Department of Clinical Biochemistry, Faculty of Medical Sciences, Tarbiat Modares University, Tehran, Iran.
Journal of gastroenterology and hepatology
|March 3, 2025
概括
肝脏中NADPH氧化酶4 (NOX4) 表达的增加在肝细胞癌 (HCC) 发展过程中先于其他氧化应激和纤维化标志物. 这项研究跟踪了NOX4和氧化应激标记在HCC的小鼠模型中.
科学领域:
- 肝细胞癌研究 肝细胞癌研究
- 氧化应激机制 氧化应激机制
- 生物标志物发现发现
背景情况:
- 肝细胞癌 (HCC) 是一种由氧化应激驱动的复杂慢性疾病,导致纤维化,肝硬化和恶性瘤.
- 了解HCC发育过程中的序列分子和生化变化对于阐明其病变发生至关重要.
研究的目的:
- 在小鼠模型中评估NADPH氧化酶4 (NOX4) 表达和氧化应激在HCC进展期间的变化.
- 为了评估纤维化血清指标,N终端型III原蛋白 (PIIINP) 与HCC进展的相关性.
主要方法:
- 甲基氨酸 (DEN) 和巴比 (PB) 用于诱导C57/bl6小鼠的HCC.
- 小鼠被分为对照组,PB,DEN和HCC组,在2,4和7个月时采集样本.
- 分析了肝脏组织和血液的NOX4mRNA/蛋白质,血清PIIINP,总抗氧化能力 (TAC),总氧化应激和谷氨 (GSH).
主要成果:
- 在HCC诱导早期,NADPH氧化酶4 (NOX4) 蛋白表达和肝 NOX4 特定的mRNA水平显著增加.
- 循环纤维化标志物PIIINP和总氧化应激水平与HCC诱导同时上升.
- 总抗氧化能力 (TAC) 和谷氨 (GSH) 水平在HCC进展过程中随着时间的推移而增加.
结论:
- 肝脏NOX4表达的增加是一个早期事件,在HCC发育中先于其他氧化应激因素和纤维化标志物.
- 这些发现突显了NOX4在HCC病原发生的早期阶段的作用.
- NOX4可能成为HCC的潜在早期诊断或治疗点.
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