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Therapeutic potential of HIV nosode 30c as evaluated in A549 lung cancer cells

机译：在A549肺癌细胞中评估的HIV Nosode 30c的治疗潜力

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Objectives To examine if HIV nosode in 30c dilution (HIV 30c) has therapeutic potential against lung cancer cells (A549) as compared to WRL-68 normal cells and to elucidate its possible molecular mechanism of action on DNA replication and apoptosis. Methods Effects of HIV 30c were thoroughly tested for its possible anticancer potential on A549?cells (lung cancer); WRL-68 normal liver cells served as control. Three doses, one at LD50 and two below LD-50, were used. Proliferation, migration and senescence assays were made and generation of reactive oxygen species (ROS) studied by routine techniques. The ability of HIV 30c to induce apoptosis in A549?cells and its possible signalling pathway were determined using immunoblots of relevant signal proteins and confocal microscopy, including studies on telomerase reverse transcriptase (TERT) and topoisomerase II (Top II) activities, intimately associated with cell division and DNA replication. Results HIV 30c prevented cancer cell proliferation and migration, induced pre-mature senescence, enhanced pro-apoptotic signal proteins like p53, bax, cytochrome c, caspase-3 and inhibited anti-apoptotic signal proteins Bcl2, TERT and Top II, changed mitochondrial membrane potential and caused externalization of phosphatidyl serine. Thus, it induced apoptosis as also evidenced from increase in cells with distorted membrane morphology, nuclear condensation, DNA fragmentation, and ROS, typical of apoptosis in progress. Conclusion HIV 30c nosode has therapeutic potential for inducing cytotoxic effects on A549?cells as manifested by changes in nuclear condensation, DNA fragmentation, ROS generation and MMP, and for its inhibitory action on cell proliferation, cell migration, expression of telomerase reverse transcriptase and Top II genes, and increasing expression of pro-apoptotic genes. Graphical abstract Display Omitted Highlights ? HIV nosode in 30th centesimal dilution induces apoptosis in cancer cells. ? It acts by inhibiting cell proliferation and migration in A549 cells. ? It down-regulates expression of TERT and topoisomerase II enzymes. ? It induces conformational changes in DNA with associated senescence.
机译：与WRL-68正常细胞相比，检查30C稀释（HIV 30C）中HIV鼻的目标是否具有针对肺癌细胞的治疗潜力（A549），并阐明了其对DNA复制和凋亡的作用分子机制。 HIV 30C的方法对其在A549？细胞（肺癌）上的可能抗癌潜力进行了彻底测试; WRL-68正常肝细胞用作对照。使用了三剂，其中1剂在LD50，两剂使用LD-50以下。进行了增殖，迁移和衰老测定，并通过常规技术研究了活性氧（ROS）。使用相关信号蛋白和共聚焦显微镜的免疫印迹确定HIV 30C在A549？细胞中诱导凋亡及其可能的信号通路的能力，包括有关端粒酶逆转录酶（TERT）和拓扑异构酶II（TOP II）活动的研究，与之紧密相关。细胞分裂和DNA复制。结果HIV 30C防止了癌细胞的增殖和迁移，诱导的成熟衰老，增强的促凋亡信号蛋白（如p53，Bax，Bax，cytothrome C，Caspase-3），抑制抗凋亡信号蛋白BCL2，TERT和TOP II，改变了线粒体膜膜膜，潜力并导致磷脂酰丝氨酸的外部化。因此，它诱导了凋亡，这也是由于膜形态扭曲，核凝结，DNA碎片和ROS的细胞增加而证明的，这是进展中凋亡的典型。结论HIV 30C鼻音具有治疗潜力，可以对A549？细胞诱导细胞毒性作用，这表现为核凝结，DNA碎片，ROS的产生和MMP的变化以及其对细胞增殖的抑制作用，细胞迁移，细胞迁移，端粒酶逆转录酶和顶部转录酶的表达以及顶部的表达II基因，以及促凋亡基因的表达增加。图形抽象显示省略了亮点？ 30世纪稀释度中的HIV鼻道诱导癌细胞凋亡。 ？它通过抑制A549细胞中的细胞增殖和迁移来起作用。 ？它下调了TERT和拓扑异构酶II酶的表达。 ？它诱导与相关衰老的DNA构象变化。

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