木犀草素调控NK细胞对胃癌细胞凋亡及PI3K/AKT信号通路的影响OA

Objective To investigate whether luteolin induces apoptosis of gastric cancer cells by regulating natural killer(NK)cell activity,and to clarify its influence on the phosphatidylinositol 3-kinase(PI3K)/protein kinase B(AKT)signaling pathway and the underlying mechanisms.Methods NK cells were divided into NK cell group and luteolin-treated group.Cell proliferation was detected by cell counting kit-8(CCK-8),and cell apoptosis was detected by flow cytometry.NK cells and gastric cancer cells were co-cultured and divided into blank group and luteolin group.The expression of NK cell activating receptors was detected by RT-qPCR.Cell proliferation was detected by CCK-8,cell apoptosis was detected by flow cytometry,and the expression of PI3K/AKT signaling pathway proteins was detected by Western blot.Results Luteolin treatment improved the biological characteristics of NK cells.Compared with the control group,the proliferation rate of NK cells increased,the apoptosis rate decreased,and the mRNA expression levels of NKp46,NKG2D,and CD226 were upregulated(P<0.05).In the functional validation experiment,the luteolin group showed a significant anti-gastric cancer effect.The proliferation of gastric cancer cells was inhibited in a time-dependent manner(P<0.05),and the apoptosis rate was significantly increased(P<0.05).Further mechanistic studies revealed that this anti-tumor effect may be related to the inactivation of the PI3K/AKT signaling pathway.Luteolin treatment reduced the protein expression levels of PI3K,p-PI3K,AKT,and p-AKT in gastric cancer cells(P<0.05).Conclusion Luteolin can effectively inhibit the progression of gastric cancer and suppress the PI3K/AKT signaling pathway,and its mechanism may be related to enhancing NK cell activity.