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. Purpose 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.