Inhibiting inflammatory processes or eliminating inflammation represents a logical role in the suppression and treatment strategy of cancer. Several studies have shown that anti-inflammatory drugs (NSAIDs) act as anticancer agents while reducing metastases and mortality rate. NSAIDs are seriously limited by their side effects and toxicity, which can become cumulative with their long-term administration for chemoprevention. In the current ex vivo / in vitro study, the genotoxicity mechanisms of NSAIDS in bulk and nanoparticle forms allowed a strategy to prevent and minimise the damage in human lymphocytes. When compared to their bulk forms, acetylsalicylic acid (Aspirin) nano and ibuprofen nano (IBU N), both NSAIDs in 500 µg/ml concentration significantly decreased DNA damage measured by alkaline comet assay. Micronuclei (MNi) frequency also decreased after ASP N (500 µg/ml), ASP B (500 µg/ml) and IBU N (200 µg/ml) in prostate cancer patients and healthy individuals, however, the ibuprofen bulk (200 µg/ml) showed a significant increase in MNi formation in lymphocytes from healthy and prostate cancer patients when compared to the respective untreated lymphocytes. These findings suggest that a reduction in particle size had an impact on the reactivity of the drug, further emphasising the potential of nanoparticles to improve the current treatment options.

抑制炎症过程或消除炎症代表了癌症抑制和治疗策略中的合乎逻辑的作用。多项研究表明，抗炎药 (NSAID) 可作为抗癌剂，同时减少转移和死亡率。NSAIDs 受到其副作用和毒性的严重限制，这些副作用和毒性会随着它们长期给药以进行化学预防而累积。在目前的离体/体外研究表明，散装和纳米颗粒形式的 NSAIDS 的基因毒性机制允许采用一种策略来预防和最大限度地减少人类淋巴细胞的损伤。与其本体形式乙酰水杨酸（阿司匹林）纳米和布洛芬纳米（IBU N）相比，浓度为 500 µg/ml 的两种 NSAID 均显着降低了碱性彗星试验测量的 DNA 损伤。在前列腺癌患者和健康个体中，在 ASP N (500 µg/ml)、ASP B (500 µg/ml) 和 IBU N (200 µg/ml) 后，微核 (MNi) 频率也降低，然而，布洛芬本体 (200 µg/ml) /ml) 显示与相应的未处理淋巴细胞相比，来自健康和前列腺癌患者的淋巴细胞中 MNi 形成显着增加。这些发现表明粒径的减小对药物的反应性有影响，