Liposome Nanoparticles Encapsulating Dehydrocameline Inhibit Cyclooxygenase-2 Expression and Reduce Inflammatory Response in Gastric Cancer Mice

Background: Dehydrokoline has a wide range of pharmacological activities and exhibits anti-tumor potential effects in a variety of cancer types. Whether it plays a role in gastric cancer remains unclear. Objectives: This study aims to explore the mechanism by which liposome nanoparticles (Harmine NPs) coated with “dehydrocardamine” inhibit COX-2 expression by regulating the PTEN/Akt signaling pathway, thereby alleviating the inflammatory response in mice with gastric cancer and providing a new strategy for targeted therapy of gastric cancer. Materials and Methods: Mice suffering from gastric cancer were used as models, and Harmine NPs were further prepared and used in experiments to observe the anti-inflammatory response in gastric cancer, explore its effect on PTEN/Akt, and analyze its role in the regulation of COX-2. Results: We successfully prepared the Harmine NPs nanocomposite, and the model group was raised for 12 weeks for subsequent animal experiments. The inflammatory factor, Harmine NPs, in the group of mice showed a better improvement in inflammation. Their mucosal muscle layer cells were evenly arranged. While the levels of inflammatory response were reduced, their COX-2 expression and genes and proteins related to the PTEN/Akt signaling pathway were also inhibited. Using SF1670 based on Harmine NPs, it was found that the inhibitory effect of Harmine NPs on PTEN protein expression was reversed. VO-OHpic simulated the inactivation of PTEN and found that the anti-inflammatory effect of Harmine NPs was amplified. After celecoxib, it was confirmed that Harmine NPs can inhibit the expression of COX-2 through the PTEN/ Akt signaling pathway to reduce the inflammatory response in gastric cancer mice. Conclusion: Harmine NPs are a new type of complex with anti-inflammatory and anti-cancer effects and are expected to become an effective strategy for the treatment of gastric cancer by inhibiting the PTEN/Akt signaling pathway and the COX-2 expression. This treatment method shows potential benefits in the management of gastric cancer inflammation and provides an important theoretical basis for the treatment of gastric cancer inflammation.