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    2-十二烷基-6-甲氧基-2,5-二烯-1,4-环己二酮对Lewis肺癌小鼠的抑瘤作用研究

    Tumor inhibitory effect of 2-dodecyl-6-methoxy-2, 5-diene-1, 4-cyclohexanedione on Lewis lung cancer mice

      摘要
    • 摘要: 目的：研究杨桃根提取物2-十二烷基-6-甲氧基-2, 5-二烯-1, 4-环己二酮（DMDD）对Lewis肺癌小鼠的抑瘤作用及其可能机制。方法：以C57BL/6小鼠构建Lewis肺癌小鼠皮下移植瘤模型，随机分为模型组、顺铂组和DMDD低、中、高剂量组，每组8 只。给药14 d 后，计算抑瘤率和脏器指数。采用酶联免疫吸附试验（ELISA）法检测移植瘤组织中炎症因子〔白介素-1β（IL-1β）、白介素-6（IL-6）、肿瘤坏死因子-α（TNF-α）〕水平，苏木精-伊红（HE）染色法观察移植瘤组织病理学改变，western blotting 法检测移植瘤组织B-淋巴细胞瘤基因-2（Bcl-2）、Bcl-2 相关X 蛋白（Bax）、核因子（NF）-κB p65（p65）和磷酸化p65（p-p65）蛋白表达水平。结果：DMDD 低、中、高剂量组和顺铂组瘤体生长缓慢，抑瘤率分别为51.08%、39.81%、46.92%、56.98%。DMDD高剂量组肺脏指数、脾脏指数与模型组比较，差异均有统计学意义（P< 0.01）。与模型组比较，DMDD各剂量组IL-1β、IL-6、TNF-α 水平均降低（P< 0.05）。给予DMDD 后坏死区域明显，细胞排列疏松，细胞核固缩。与模型组比较，DMDD 中、高剂量组和顺铂组Bcl-2 蛋白相对表达量明显降低（P< 0.05），DMDD 各剂量组和顺铂组Bax 蛋白相对表达量升高，而p-p65/p65比值显著降低（均P< 0.05）。结论：DMDD可抑制Lewis肺癌小鼠肿瘤生长，可能通过调控NF-κB信号通路诱导肺癌细胞凋亡，从而发挥抗肿瘤作用。

       

      Abstract: Objective:To study the tumor inhibitory effect of 2-dodecyl-6-methoxy-2, 5-diene-1, 4-cyclohexanedione (DMDD) isolated from the root of Averrhoa carambola L.on Lewis lung cancer mice and its possible mechanism.Methods:A subcutaneous transplantation tumor model of Lewis lung cancer mice was constructed with C57BL/6 mice and randomly divided into model group, cisplatin group, low-dose DMDD group, mediumdose DMDD group and high-dose DMDD group, with 8 mice in each group.After 14 days of administration, tumor inhibitory rate and organ index were calculated.The levels of inflammatory factorsinterleukin-1(IL-1), interleukin-6 (IL-6) and tumor necrosis factor-α (TNF-α) in transplanted tumor tissues were detected by enzymelinked immunosorbent assay (ELISA).Hematoxylin-eosin (HE) staining was used to observe the pathological changes of transplanted tumor tissue, and western blotting was used to detect B-cell lymphoblastoma gene-2(Bcl-2), Bcl-2-associated X protein (Bax), nuclear factor (NF)-κB p65 (p65) and phosphorylated p65 (p-p65) protein expression levels in tumor tissues.Results:The tumor growth was slow in all DMDD groups and the cisplatin group, and the tumor inhibitory rates were 51.08%, 39.81%, 46.92%and 56.98%, respectively.There were statistically significant differences in the lung index and spleen index between the DMDD high-dose group and the model group (P< 0.01).Compared with the model group, the levels of IL-1, IL-6 and TNF-α in all DMDD groups decreased (P< 0.05).After administration of DMDD, the necrotic area was obvious, the cell arrangement was loose, and the nucleus was solidified.Compared with the model group, the relative expression levels of Bcl-2 protein in medium-dose and high-dose DMDD groups significantly decreased, as well as the cisplatin group (P< 0.05), the relative expression levels of Bax protein in all DMDD dose groups and the cisplatin group increased, while the P-P65/p65 ratio significantly decreased (all P< 0.05).Conclusion:DMDD can inhibit tumor growth in Lewis lung cancer mice, possibly by regulating the NF-κB signaling pathway to induce apoptosis in lung cancer cells, thereby exerting an anti-tumor effect.

       

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