柴芪益肝颗粒通过抑制PI3K/AKT和ERK信号通路延缓肝细胞癌进展OA

Objective To investigate the effect and mechanism of Chaiqi Yigan Granules(柴芪益肝颗粒)on H22 hepatocel-lular carcinoma bearing mice.Methods Fifty specific pathogen-free male Kunming mice were used to establish H22 hepatoma tumor-bearing mouse models by subcutaneous injection of H22 hepatoma cells into the left armpit.After the models were suc-cessfully constructed,the mice were randomly divided into model group,Chaiqi Yigan Granules low-dose group,Chaiqi Yigan Granules medium-dose group,Chaiqi Yigan Granules high-dose group and sorafenib group by random number table method(10 per group).The samples were collected 14 days after intragastric administration according to the group.HE staining was used to observe the pathological morphological changes of tumor tissues.TUNEL staining was used to observe the degree of apoptosis in tumor tissues.RT-qPCR was used to detect the mRNA expressions of apoptosis-related genes B-cell lymphoma 2(Bel-2),Bel-2 associated X protein(Bax)and activated cysteine proteinase 3(Caspase-3).The expressions of apoptosis-related pro-teins Bel-2,Bax,Caspase-3,invasion and migration proteins N-cadherin,MMP7,Vimentin,E-cadherin and PI3K/AKT/ERK signaling pathway were detected by Western blot.The expression of Caspase-3 in tumor tissues was detected by immunohis-tochemistry method.Results Compared with the model group,Chaiqi Yigan Granules could effectively delay the progression of tumor,promote the apoptosis of tumor cells,up-regulated mRNA and protein expressions of Bax and Caspase-3,down-regula-ted mRNA and protein expressions of Bel-2,enhanced the protein expression of E-cadherin,decreased the protein expressions of N-cadherin,MMP7 and Vimentin in tumor tissue and inhibited the protein expression of PI3K/AKT/ERK signaling pathway.Conclusion Chaiqi Yigan Granules may promote tumor cell apoptosis and inhibit the epithelial-mesenchymal transition by inhib-iting PI3K/AKT and ERK signaling pathways,thus delaying the progression of hepatocellular carcinoma.