Abstract

In order to explore the anticancer mechanism of bile acid receptor TGR5 in lung cancer mouse models, healthy C57BL/6J mice of the wild-type and the TGR5 gene knockout type and human lung adenocarcinoma cell line A549 were selected as test system to construct animal models. The mouse models were used to observe the inhibitory effects of bile acid receptor TGR5 on lung cancer and related indicators, inflammatory mediators and mRNA expression levels. Through comparisons between the genes of wild-type mice and TGR5 knockout mice, it was found that the expression levels of IP-10, IL-1β, IFN-γ, CCL4, CXCL2, and CCL3 were significantly higher in the TGR5 knockout model group than those in the wild-type control group. Analysis of the effects of TGR5 on the proliferation of lung adenocarcinoma cells, A549, revealed that the RGT5 agonist could effectively inhibit proliferation of lung cancer cells. Analysis of the effects of TGR5 on apoptosis of lung adenocarcinoma cells A549, indicated that after adding DY240 or INT777 agonist, the level of cell apoptosis was significantly increased compared to the control group. Analysis of the effects of TGR5 on NF-κB signalling pathway showed that inactivating TGR5 could effectively inhibit the expression and phosphorylation of inflammatory factors related to signalling pathways in lung cancer cells. Therefore, it was found that the intervention with TGR5 agonist could effectively inhibit the proliferation of lung cancer cells, which achieved the expected results. Despite the deficiencies in the research process, it has provided a certain basis and ideas for subsequent research on exploring the treatments of lung cancer more accurately. Thus, the study is of great significance.