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柴芪益肝颗粒改善肝细胞癌的作用机制预测及验证
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| 篇名： | 柴芪益肝颗粒改善肝细胞癌的作用机制预测及验证 |
| TITLE： | Prediction and verification of the mechanism of Chaiqi yigan granules improving hepatocellular carcinoma |
| 摘要： | 目的 预测柴芪益肝颗粒改善肝细胞癌（HCC）的作用机制，并进行验证。方法采用网络药理学方法预测柴芪益肝颗粒改善HCC的信号通路。采用腋下注射肝癌细胞H22的方法构建肝癌移植瘤模型小鼠，将造模成功的小鼠随机分为模型组（生理盐水）、索拉非尼组（阳性对照，50mg/kg）和柴芪益肝颗粒低、中、高剂量组（24.83、49.66、99.32g/kg），每组10只。各组小鼠灌胃相应药液或生理盐水，每日1次，连续14d。末次给药后，观察小鼠肿瘤组织病理学形态，采用免疫组化法检测小鼠肿瘤组织中细胞核增殖抗原Ki-67表达，采用Westernblot法检测小鼠肿瘤组织中上皮间质转化[N-钙黏蛋白（N-cadherin）、E-钙黏蛋白（E-cadherin）、波形蛋白（Vimentin）、基质金属蛋白酶7（MMP7）]和丝裂原活化蛋白激酶（MAPK）信号通路[p38MAPK、磷酸化p38MAPK、c-Jun氨基末端激酶（JNK）、磷酸化JNK、细胞外调节蛋白激酶1/2（ERK1/2）、磷酸化ERK1/2]相关蛋白表达。结果网络药理学结果显示，代谢通路、癌症通路、MAPK信号通路等可能是柴芪益肝颗粒改善HCC的关键信号通路。动物实验验证结果显示，模型组小鼠肿瘤组织中肿瘤细胞密集、生长状态旺盛；与模型组比较，柴芪益肝颗粒高剂量组小鼠肿瘤组织中肿瘤细胞密度降低，肿瘤组织中Ki-67、N-cadherin、MMP7、Vimentin蛋白表达水平和ERK1/2、JNK蛋白磷酸化水平均显著降低（P＜0.05），E-cadherin蛋白表达水平显著升高（P＜0.05），p38MAPK蛋白磷酸化水平升高但差异无统计学意义（P＞0.05）。结论柴芪益肝颗粒可通过调控MAPK信号通路，抑制上皮间质转化，从而抑制肿瘤细胞侵袭和转移，进而发挥改善HCC的作用。 |
| ABSTRACT： | OBJECTIVE To predict and validate the mechanisms of Chaiqi yigan granules （CQYG） improving hepatocellular carcinoma （HCC）. METHODS The signaling pathways of CQYG intervention in HCC were predicted using network pharmacology. A mice model of transplanted hepatocellular carcinoma was established by injecting H22 hepatoma cells into the axilla. Successfully modeled mice were randomly divided into model group （normal saline）， sorafenib group （positive control， 50 mg/kg）， and CQYG low-， medium- and high-dose groups （24.83， 49.66， 99.32 g/kg）， with 10 mice in each group. Mice in each group were administered the corresponding drug solution or normal saline intragastrically， once a day， for 14 consecutive days. After last administration， pathological morphological changes in the tumor tissues of mice were observed in each group. Immunohistochemical staining was performed to detect the expression of the nuclear proliferation antigen Ki-67 in tumor tissues of mice. Western blot assay was used to measure the expression of proteins related to epithelial-mesenchymal transition （EMT） [N-cadherin， E-cadherin， Vimentin， matrix metalloproteinase 7 （MMP7）] and the mitogen-activated protein kinase （MAPK） signaling pathway [p38 MAPK， phosphorylated p38 MAPK， c-Jun N-terminal kinase （JNK）， phosphorylated JNK， extracellular regulated protein kinase 1/2 （ERK1/2）， phosphorylated ERK1/2] in tumor tissue of mice. RESULTS Network pharmacology analysis revealed that metabolic pathways， pathways in cancer， and the MAPK signaling pathway were key signaling pathways through which CQYG exert their anti-hepatocellular carcinoma effects. In animal experiments， the tumor tissues of mice in the model group exhibited dense tumor cells and vigorous growth. Compared with model group， CQYG high-dose group showed a decreased density of tumor cells in the tumor tissues of mice. Moreover， the expression levels of Ki-67， N-cadherin， MMP7 and Vimentin proteins， along with the phosphorylation levels of ERK1/2 and JNK proteins， were all significantly reduced （ P ＜0.05）. The expression level of E-cadherin protein was significantly increased （ P ＜0.05）， the phosphorylation level of p38 MAPK protein was increased， the difference was not statistically significant （ P ＞0.05）. CONCLUSIONS CQYG can inhibit EMT by regulating the MAPK signaling pathway， thereby suppressing tumor cell invasion and metastasis and ultimately exerting a therapeutic effect in improving HCC. |
| 期刊： | 2026年第37卷第05期 |
| 作者： | 马贵萍；张远杰；周怡驰；吕锦珍；王聪慧；卢芬萍；刘博文；冉云；胡世平 |
| AUTHORS： | MA Guiping， ZHANG Yuanjie，ZHOU Yichi，LYU Jinzhen，WANG Conghui，LU Fenping，LIU Bowen，RAN Yun，HU Shiping |
| 关键字： | 柴芪益肝颗粒；肝细胞癌；MAPK信号通路；上皮间质转化；网络药理学 |
| KEYWORDS： | Chaiqi yigan granules； hepatocellular carcinoma； MAPK signaling pathway； epithelial-mesenchymal transition； |
| 阅读数： | 1 次 |
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