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芪玉三龙汤对荷瘤小鼠肿瘤组织PI3K/Akt/mTOR通路分子表达的影响 被引量:11

Effects of Qiyu Sanlong Decoction on expression of molecular affiliated to PI3K/Akt/mTOR pathway on tumor in the mice burdened lung carcinoma
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摘要 目的:进一步研究芪玉三龙汤对荷瘤小鼠移植瘤PI3K/Akt/mTOR通路相关分子表达的影响。方法:无菌培养LLC细胞,收集细胞悬液接种C57BL/6小鼠腋部皮下构建肺癌模型,接种第11天将荷瘤小鼠随机分为6组:模型组,化疗组,芪玉三龙汤高、中、低剂量组,联合组,每组8只。称取瘤质量,计算抑瘤率;RT-qPCR法检测肿瘤组织PIK3CA、Akt、mTOR mRNA转录水平;Western blot法检测肿瘤组织p-Akt、p-mTOR、PDK1、p-PDK1蛋白表达水平。结果:芪玉三龙汤可温和抑制肺肿瘤生长,以高剂量组抑瘤作用最优,但无明显量效关系,与化疗药联用暂无明显协同作用;芪玉三龙汤可下调PIK3CA、Akt、mTOR基因转录水平并且同时下调p-Akt、p-mTOR、PDK1、p-PDK1蛋白表达。结论:芪玉三龙汤温和的抑瘤作用与调控PI3K/Akt/mTOR信号通路相关。 Objective: To further observe the effects of Qiyu Sanlong Decoction(QYSL) on expression of molecular affiliated to PI3K/Akt/mTOR pathway on tumor in the mice burdened lung carcinoma.Methods: LLC cells were cultured aseptically,and the lung cancer model was established by inoculating cell suspension in C57 BL/6 mice.The tumor-bearing mice were randomly divided into six groups on 11 th day which respectively were model group,chemotherapy group,QYSL high,medium,low dose group,combined group and each group included 8 mice.The weight of tumor was measured and tumor inhibition rate was calculated.The m RNA expressions of PIK3 CA,Akt and mTOR were measured by RT-qPCR,and the expressions of p-Akt,p-mTOR,PDK1,and p-PDK1 in tumor tissues were measured by Western blot.Results: QYSL could inhibit the growth of lung tumor mildly,especially in its high dose group.But there was no significant dose-effect relationship,and there was no obvious synergistic effect with chemotherapy drug; QYSL could reduce gene transcription levels of PIK3 CA,Akt,MTOR and simultaneously down-regulated protein expressions of p-Akt,p-mTOR,PDK1,p-PDK1.Conclusion: The moderate tumor suppression effect of QYSL is related to its regulation on PI3 K/Akt/mTOR signaling pathway.
出处 《中华中医药杂志》 CAS CSCD 北大核心 2017年第12期5358-5361,共4页 China Journal of Traditional Chinese Medicine and Pharmacy
基金 安徽省自然科学基金面上项目(No.1708085MH197)~~
关键词 芪玉三龙汤 肺癌 PI3K/Akt/m TOR Qiyu Sanlong Decoction Lung cancer PI3K/Akt/mTOR
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