文献类型：期刊文献

中文题名：参芪抑瘤方联合顺铂对H22肝癌荷瘤小鼠抑瘤作用的研究

英文题名：Study on the anti-tumor effect of Shenqi Yiliu decoction combined with cisplatin on H22 liver cancer-bearing mice

作者：杨玉萍[1,2];段永强[2,3];梁建庆[1,2];白敏[1,2];冯鑫[1,2];曹力仁[1,2];刘自由[1,2]

第一作者：杨玉萍

机构：[1]甘肃中医药大学基础医学院,甘肃兰州730000;[2]甘肃省实验动物行业技术中心,甘肃兰州730000;[3]宁夏医科大学中医学院,宁夏回族自治区银川750004

第一机构：甘肃中医药大学基础医学院（敦煌医学研究所）

年份：2023

卷号：39

期号：14

起止页码：2069

中文期刊名：中国临床药理学杂志

外文期刊名：The Chinese Journal of Clinical Pharmacology

收录：CSTPCD;;北大核心:【北大核心2020】；CSCD:【CSCD2023_2024】；

基金：甘肃省人才创新创业项目扶持基金资助项目(2015-RC-24);甘肃省发改委2013年第十一批建设项目计划基金资助项目(2305142201);甘肃省中医药研究中心开放课基金资助项目(zyzx-2020-zx20)。

语种：中文

中文关键词：参芪抑瘤方;顺铂;肝癌;c-Jun氨基末端激酶信号通路

外文关键词：Shenqi Yiliu decoction;cisplatin;H22 hepatocellular carcinoma;c-Jun amino-terminal kinase signaling pathway

摘要：目的探讨参芪抑瘤方联合顺铂对H22肝癌荷瘤小鼠的抑瘤作用及其机制。方法用雄性昆明小鼠复制H22肝癌荷瘤小鼠模型,另取10只正常小鼠作为空白组。将模型鼠随机分为模型组(0.9%NaCl)、顺铂组(2.5×10^(-3)g·kg^(-1)·3 d^(-1)顺铂)及低、中、高剂量(13.52、27.03和54.06 g·kg^(-1)·d^(-1)参芪抑瘤方)联合顺铂(顺铂2.5×10^(-3)g·kg^(-1)·3 d^(-1))组,干预治疗13 d。用苏木精-伊红(HE)染色和细胞凋亡染色(TUNEL)法观察肿瘤病理变化及凋亡情况;用实时荧光定量聚合酶链反应法和蛋白质印迹法检测肿瘤组织中磷酸化c-Jun氨基末端蛋白激酶(p-JNK)、B淋巴细胞瘤-2(Bcl-2)、Bcl-2相关X蛋白(Bax)、B淋巴细胞瘤-2基因相关启动子(Bad)、半胱氨酸蛋白酶-9(Caspase-9)mRNA及蛋白的表达水平。结果模型组、顺铂组、参芪抑瘤方高剂量联合顺铂组肿瘤组织细胞凋亡率分别为(6.99±0.34)%、(33.18±3.50)%和(64.32±2.21)%,p-JNK蛋白相对表达水平分别为0.21±0.02、0.43±0.05和1.04±0.05,Bcl-2蛋白相对表达水平分别为1.60±0.01、1.36±0.05和0.47±0.01,Bax蛋白相对表达水平分别为0.31±0.03、0.45±0.03和0.99±0.02,Bad蛋白相对表达水平分别为0.34±0.02、0.66±0.03和1.10±0.03,Caspase-9蛋白相对表达水平分别为0.39±0.04、0.50±0.03和0.85±0.06;模型组的上述指标与顺铂组比较,差异均有统计学意义(均P<0.01);模型组和顺铂组的上述指标与参芪抑瘤方高剂量联合顺铂组比较,差异均有统计学意义(均P<0.01)。结论参芪抑瘤方联合顺铂能有效抑制H22肝癌荷瘤小鼠的肿瘤生长,该作用机制可能与调控JNK信号通路及相关凋亡蛋白的表达有关。
Objective To explore the tumor suppressing effect of Shenqi Yiliu(SQYL)decoction combined with cisplatin(CDDP)on H22 liver cancer tumor-bearing mice and its mechanism.Methods The H22hepatocellular carcinoma tumor-bearing mouse model was replicated using male Kunming mice,and another 10 normal mice were taken as blank group.The model mice were randomly divided into model(0.9%Na Cl),CDDP(2.5×10^(-3)g·kg^(-1)·3 d^(-1)CDDP),and SQYL-L,-M,-H+CDDP(13.52,27.03,54.06 g·kg^(-1)·d^(-1)SQYL+2.5×10^(-3)g·kg^(-1)·3 d^(-1)CDDP).Interventions were administered for 13 d.Tumor pathological changes and apoptosis were observed by hematoxylin-eosin staining(HE)and apoptosis staining(TUNEL);real-time fluorescence quantitative polymerase chain reaction and protein blotting methods were used to detected the mRNA and protein expression levels of phosphorylated c-Jun amino-terminal protein kinase(p-JNK),B lymphocytoma-2(Bcl-2),Bcl-2-associated X protein(Bax),B lymphocytoma-2 gene-associated promoter(Bad),and duck cysteine protease-9(Caspase-9)in tumor tissues.Results The apoptosis rates of tumor tissues in the model group,CDDP group and SQYL-H+CDDP group were(6.99±0.34)%,(33.18±3.50)%and(64.32±2.21)%,respectively;the relative protein expression levels of p-JNK were 0.21±0.02,0.43±0.05 and1.04±0.05,respectively;the relative protein expression levels of Bcl-2 were 1.60±0.01,1.36±0.05,0.47±0.01,respectively;the relative protein expression levels of Bax in the three groups were 0.31±0.03,0.45±0.03 and 0.99±0.02,respectively;the relative protein expression levels of Bad in the three groups were0.34±0.02,0.66±0.03 and 1.10±0.03,respectively;the relative protein expression levels of Caspase-9 were0.39±0.04,0.50±0.03 and 0.85±0.06,respectively.The above indexes in the model group were significantly different from those in the CDDP group(all P<0.01).The above indexes in the model group and CDDP group were significantly different from those in the SQYL-H+CDDP group(all P<0.01).Conclusion Shenqi Yiliu decoction combined with cisplatin effectively inhibited tumor growth in H22 hepatoma-bearing mice,and the mechanism of action may be related to the regulation of JNK signaling pathway and the expression of related apoptotic proteins.