Diethylnitrosamine (DEN) promoted by carbon tetrachloride (CCl4) forms DNA adducts inducing hepatocellular carcinoma (HCC). Plant alkaloid, harmalol, is being used as a therapeutic agent against HCC due to its accessibility and efficacy by apoptosis and inhibiting proliferation of cancer epithelial cells. Seven groups of Swiss albino mice were taken. Different stages of liver tissues and serum from various experimental groups were collected before and after harmalol treatment. The investigation was carried out by enzyme assay, bilirubin level in the blood, DNA, RNA, normal serum protein of liver tissue, and alpha-feto protein estimation of serum. Gross morphological assessment of liver, histological, and different apoptosis markers viz. p53, caspase3, and cytochrome C expression were analyzed by RT-PCR and Western blot. Harmalol (10 mg/kg B.W. per week, I.P.) for 9 weeks showed a significant reduction in hepatocellular foci, nodules, and carcinoma ultimately retaining the normal morphology. It further induces ROS-dependent apoptosis through mitochondrial cytochrome C release that induces p53 by caspase3 activation. The investigation will eventually help to develop more effective chemotherapeutic drugs from the natural source.

中文翻译：

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harmalol抑制肝细胞癌的药效

四氯化碳（CCl4）促进的二乙基亚硝胺（DEN）形成诱导肝细胞癌（HCC）的DNA加合物。由于其可通过细胞凋亡和抑制癌细胞上皮细胞增殖的功效和功效，植物生物碱，harmalol被用作抗HCC的治疗剂。取七组瑞士白化病小鼠。在接受malalol治疗之前和之后，收集了来自各个实验组的肝脏组织和血清的不同阶段。通过酶测定，血液中胆红素水平，DNA，RNA，肝组织正常血清蛋白以及血清中甲胎蛋白的估计来进行研究。肝，组织学和不同凋亡标志物的总体形态学评估。通过RT-PCR和Western印迹分析p53，caspase3和细胞色素C的表达。Harmalol（10 mg / kg体重 每周（IP）持续9周，显示肝细胞灶，结节和癌的明显减少，最终保持了正常形态。它通过线粒体细胞色素C的释放进一步诱导ROS依赖的凋亡，线粒体的细胞色素C释放通过caspase3激活诱导p53。该调查最终将有助于从天然来源开发更有效的化学治疗药物。