文献类型：期刊文献

中文题名：敦煌平胃丸及其拆方对SCG-7901胃癌荷瘤小鼠的抑瘤作用及对PI3K/Akt/mTOR信号通路的影响

英文题名：Effect of Dunhuang Pingweiwan and Its Decomposed Recipes on Tumor Inhibition and PI3K/Akt/mTOR Pathway in SCG-7901 Gastric Cancer Mice

作者：舍雅莉[1];赵晓文[1];李俊杰[1];董娟娟[1];刘永琦[1];刘喜平[1];李长天[1];李亚玲[1]

第一作者：舍雅莉

机构：[1]甘肃中医药大学敦煌医学与转化教育部重点实验室,甘肃省高校重大疾病分子医学与中医药防治研究省级重点实验室,兰州730000

第一机构：甘肃中医药大学科研实验中心（甘肃省中医药标准化技术委员会秘书处）

年份：2021

卷号：27

期号：5

起止页码：70

中文期刊名：中国实验方剂学杂志

外文期刊名：Chinese Journal of Experimental Traditional Medical Formulae

收录：CSTPCD;;北大核心:【北大核心2020】；CSCD:【CSCD2021_2022】；

基金：甘肃省高等学校产业支撑计划项目(2020C-15);甘肃省高等学校创新能力提升项目(2019A-074);敦煌医学与转化教育部重点实验室开放课题项目(DHYX14-010,DHYX18-012)。

语种：中文

中文关键词：敦煌平胃丸;胃癌;磷脂酰肌醇3-激酶(PI3K);蛋白激酶B(Akt);哺乳动物雷帕霉素靶蛋白(mTOR)

外文关键词：Dunhuang Pingweiwan;gastric cancer;phosphatidylinositol 3-kinase(PI3K);protein kinase B(Akt);mammalian target of rapamycin(mTOR)

摘要：目的:研究敦煌平胃丸及其拆方对胃癌荷瘤小鼠的抑瘤作用,并从磷脂酰肌醇3-激酶(PI3K)/蛋白激酶B(Akt)/哺乳动物雷帕霉素靶蛋白(mTOR)信号通路研究敦煌平胃丸及其拆方可能的作用机制。方法:建立SCG-7901胃癌皮下荷瘤小鼠模型,随机分为模型组,敦煌平胃丸组(14.04 g·kg^(-1)·d^(-1)),活血解毒组(6.50 g·kg^(-1)·d^(-1)),温中散寒组(3.64 g·kg^(-1)·d^(-1))和顺铂组(2 mg·kg^(-1)·d^(-1)),每组8只。接种第8天开始给药,连续10 d,隔日小鼠称体质量并观察一般情况;末次给药后次日处死小鼠,剥取肿瘤称质量,计算抑瘤率;苏木素-伊红(HE)染色观察肿瘤组织病理学变化,实时荧光定量聚合酶链式反应(Real-time PCR)和免疫组化法(IHC)分别检测肿瘤组织中PI3K,Akt,mTOR mRNA和蛋白表达情况。结果:接种第10天开始,顺铂组小鼠一般情况较差,体质量下降,模型、敦煌平胃丸、活血解毒和温中散寒组小鼠一般情况尚可,体质量增长,组间差异无统计学意义;敦煌平胃丸、活血解毒、温中散寒和顺铂组抑瘤率分别为30.74%,24.80%,4.19%和63.84%,除温中散寒组外,其余给药组瘤质量均较模型组显著降低(P<0.01),其中敦煌平胃丸与活血解毒组间差异无统计学意义;敦煌平胃丸和活血解毒组能明显降低肿瘤细胞密度,引起肿瘤细胞坏死;与模型组比较,敦煌平胃丸、活血解毒和顺铂组PI3K,Akt,mTOR mRNA和蛋白表达均明显下降(P<0.05,P<0.01),其中敦煌平胃丸与活血解毒组差异无统计学意义。结论:敦煌平胃丸及其拆方(活血解毒方)对SCG-7901胃癌荷瘤小鼠具有一定的抑瘤作用,其机制可能与下调PI3K/Akt/mTOR信号通路关键分子表达有关。
Objective:To investigate the antitumor effect and the mechanism of Dunhuang Pingweiwan and its decomposed recipes based on phosphatidylinositol 3-kinase(PI3K)/protein kinase B(Akt)/mammalian target of rapamycin(mTOR)signaling pathway in SCG-7901 gastric cancer-mice. Method: The subcutaneous tumor bearing model of SCG-7901 gastric cancer in mice was established,and the the mice were randomized into model group,Dunhuang Pingweiwan group(14.04 g·kg^(-1)·d^(-1)),Huoxue Jiedu group(6.50 g·kg^(-1)·d^(-1)),Wenzhong Sanhan group(3.64 g·kg^(-1)·d^(-1))and cisplatin group(2 mg·kg^(-1)·d^(-1)),with 8 mice in each group. From the 8 thday of inoculation,the mice were administered for 10 consecutive days. The mice were weighed and the general conditions were observed every other day. On the next day of the last administration,the mice were sacrificed,and the tumor was removed and weighed to calculate the anti-tumor rate. The histopathological changes were observed by hematoxylin-eosin(HE)staining,and the mRNA and protein expressions of PI3K,Akt,and mTOR in tumor tissues were detected by real-time polymerase chain reaction(Real-time PCR)and immunohistochemistry(IHC),respectively. Result: From the 10 thday of inoculation,the mice in cisplatin group were generally in poor condition and their body mass decreased. The mice in model group,Dunhuang Pingweiwan group,Huoxue Jiedu group and Wenzhong Sanhan group were generally fair,and their body mass increased without significant difference among groups. The tumor inhibition rates of Dunhuang Pingweiwan,Huoxue Jiedu,Wenzhong Sanhan and cisplatin groups were 30.74%,24.80%,4.19% and 63.84%,respectively.Except for Wenzhong Sanhan group,tumor weight of the other treatment groups was significantly lower than that of the model group(P<0.01),and there was no significant difference between the Dunhuang Pingweiwan and Huoxue Jiedu group. Dunhuang Pingweiwan and Huoxue Jiedu group could significantly reduce tumor cell density and cause tumor cell necrosis. Compared with the model group,the expressions of PI3K,Akt,and mTOR mRNA and protein in the Dunhuang Pingweiwan,Huoxue Jiedu and cisplatin groups significantly decreased(P<0.05,P<0.01),and there was no significant difference between the Dunhuang Pingweiwan group and Huoxue Jiedu group. Conclusion: Dunhuang Pingweiwan and its decomposed recipes(Huoxue Jiedu)have a certain anti-tumor effect on the SCG-7901 gastric cancer-mice,and the mechanism may be related to the downregulation of key molecules in the PI3K/Akt/mTOR signaling pathway.