The most frequent type of primary liver cancer is hepatocellular carcinoma (HCC), accounting for approximately 90% of primary liver cancers and a third leading cause of cancer deaths. In the current study, the synthesized compound 3 was re-formulated using tetraethyl orthosilicate (TEOS) with weight ratio (1:1) via sol-gel technique. The prepared material has been examined using Fourier transform infrared spectroscopy (FTIR), energy dispersive X-ray elemental analysis (EDX), and scanning and transmission electron microscopes (SEM and TEM). Herein, we investigate the mode of action of 3 as potent anti-liver cancer in vivo as normal and nano-forms. Rats were given a single dosage of 50 mg/kg b.wt. of HCC through an intraperitoneal injection (ip). A single dosage of CCl4 (2 ml/kg IP) was also given to rats 2 weeks later. Several liver, tumor and oxidative stress biomarkers were detected including liver enzymes; alanine and aspartate aminotransferases (ALT and AST), alkaline phosphatse (ALP), gamma glutamyl transferase (GGT), glutathione (GSH), lipid peroxide (MDA), catalase (CAT), superoxide dismutase (SOD), total antioxidant capacity (TAC), α-fetoprotein and α-L-Fucosidase. Hepatic pathological pictures were also performed for the documentation of the presence of HCC and supported the biochemical results. Moreover, the DNA damage in liver tissues of male rats using comet assay was studied. The results showed that the HePG2 (− ve) group of rats exhibited a significant reduction (P < 0.05) in DNA damage values (9.30 ± 0.89) relative to other treatment groups. Nevertheless, the DNA damage values in the HePG2 (+ ve) and 5-flurouracil groups were significantly higher (P < 0.01) compared to the HePG2 (− ve) group. Additionally, HePG2 (coated 3) and HePG2 (3) groups exhibited significant decrease in the DNA damage compared to those in HePG2 (+ ve) group.

中文翻译：

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磺脲类衍生物作为一种新的游离和纳米涂层形式的肝癌化疗药物的生化和组织病理学研究

最常见的原发性肝癌类型是肝细胞癌 (HCC)，约占原发性肝癌的 90%，是癌症死亡的第三大原因。在目前的研究中，合成的化合物 3 通过溶胶-凝胶技术使用重量比 (1:1) 的原硅酸四乙酯 (TEOS) 重新配制。使用傅里叶变换红外光谱 (FTIR)、能量色散 X 射线元素分析 (EDX) 以及扫描和透射电子显微镜 (SEM 和 TEM) 对制备的材料进行了检查。在此，我们研究了 3 作为有效抗肝癌的体内正常和纳米形式的作用方式。给大鼠单次剂量为 50 mg/kg b.wt。通过腹膜内注射 (ip) 治疗 HCC。2 周后也给大鼠单剂量的 CCl4 (2 ml/kg IP)。几个肝脏，检测到包括肝酶在内的肿瘤和氧化应激生物标志物；丙氨酸和天冬氨酸氨基转移酶（ALT和AST）、碱性磷酸酶（ALP）、γ谷氨酰转移酶（GGT）、谷胱甘肽（GSH）、过氧化脂质（MDA）、过氧化氢酶（CAT）、超氧化物歧化酶（SOD）、总抗氧化能力（TAC） )、甲胎蛋白和 α-L-岩藻糖苷酶。还进行了肝脏病理图片以记录 HCC 的存在并支持生化结果。此外，使用彗星试验研究了雄性大鼠肝组织中的DNA损伤。结果表明，相对于其他治疗组，HePG2 (− ve) 组大鼠的 DNA 损伤值 (9.30 ± 0.89) 显着降低 (P < 0.05)。然而，HePG2 (+ ve) 和 5-氟尿嘧啶组的 DNA 损伤值显着升高（P < 0. 01) 与 HePG2 (− ve) 组相比。此外，与 HePG2 (+ ve) 组相比，HePG2 (涂层 3) 和 HePG2 (3) 组的 DNA 损伤显着减少。