Canine mammary tumors are one of the most common causes of cancer-related death in female dogs,challenging traditional surgical therapies due to their high recurrence and metastasis.The natural compound Ole is strongly associated with a variety of phenomena,such as increased longevity,reduced disease incidence and mortality.However,its effect on canine mammary tumors is unclear.Therefore,the following experiments were conducted to investigate whether Ole has an effect on the development of canine mammary tumors:The effects of Ole at different concentra-tions on CHMm cell viability,migration ability,apoptosis,expression levels of corresponding pro-teins Bax and BCL-2 and mRNA expression of tumor-related genes were detected by scratch test,flow cytometry,RT-qPCR and protein western blot,and the mechanism of action was also ex-plored.The results showed that Ole activated the PI3K/AKT signaling pathway,induced phospho-rylation of related proteins,and significantly inhibited the expression levels of p-PI3K and p-AKT after applying OLE to CHMm of canine mammary tumor cells.At the same time,Ole significantly inhibited the survival,migration and proliferation of canine mammary tumor cells.In addition,the expressions of proteins Bax and BCL-2,which are closely related to apoptosis,and mRNA expres-sions of some tumor-related genes were significantly regulated,suggesting that Ole mediated PI3K/AKT signaling pathway effectively induced apoptosis of canine mammary tumor cells.This study suggests that Ole has the potential to become a key drug in the treatment of mammary canc-er,and provides a key target for the development of effective therapies against canine mammary tumors.

Canine mammary tumors are one of the most common causes of cancer-related death in female dogs,challenging traditional surgical therapies due to their high recurrence and metastasis.The natural compound Ole is strongly associated with a variety of phenomena,such as increased longevity,reduced disease incidence and mortality.However,its effect on canine mammary tumors is unclear.Therefore,the following experiments were conducted to investigate whether Ole has an effect on the development of canine mammary tumors:The effects of Ole at different concentra-tions on CHMm cell viability,migration ability,apoptosis,expression levels of corresponding pro-teins Bax and BCL-2 and mRNA expression of tumor-related genes were detected by scratch test,flow cytometry,RT-qPCR and protein western blot,and the mechanism of action was also ex-plored.The results showed that Ole activated the PI3K/AKT signaling pathway,induced phospho-rylation of related proteins,and significantly inhibited the expression levels of p-PI3K and p-AKT after applying OLE to CHMm of canine mammary tumor cells.At the same time,Ole significantly inhibited the survival,migration and proliferation of canine mammary tumor cells.In addition,the expressions of proteins Bax and BCL-2,which are closely related to apoptosis,and mRNA expres-sions of some tumor-related genes were significantly regulated,suggesting that Ole mediated PI3K/AKT signaling pathway effectively induced apoptosis of canine mammary tumor cells.This study suggests that Ole has the potential to become a key drug in the treatment of mammary canc-er,and provides a key target for the development of effective therapies against canine mammary tumors.

Objective:To explore the effect of the virulence factor OatA during Staphylococcus aureus infection.Methods: In vitro,wild type of Staphylococcus aureus USA300,OatA gene deletion strain or OatA gene complemented strain were used to infect mice bone marrow divided macrophages (BMDMs).Subsequently BMDMs were separated and the case of cell death were detected.In vivo,mice pulmonary infection model was constructed with nasal inhalation of Staphylococcus aureus.Alveolar macrophages were isolated and the case of cell death were detected.Results: In contrast to wild type and OatA gene complemented strain,OatA gene deletion strain induced severer macrophage death both in vitro and in vivo.Conclusion: The virulence factor OatA inhibits Staphylococcus aureus infection-induced macrophage death.