Mechanism Of Salidroside Inhibiting Proliferation And Migration Of Human Lung Cancer A549 Cells

Background: Global cancer data reported in the American Journal of Clinical Cancer Medicine in 2021 show that lung cancer is the second most common cancer in the world,and its fatality rate ranks the first among all cancers.Non-small cell lung cancer（NSCLC）accounts for more than 85% of all lung cancers.Therefore,it is of great significance to study the mechanism of NSCLC and explore effective intervention methods.Recent studies have shown that inflammatory responses mediated by NACHT,LRR and PYD domain protein 3（NLRP3）play an important role in the development and progression of NSCLC.Salidroside（SAL）is an active component contained in Rhodiola sachalinensis.Studies have shown that the component can inhibit the proliferation and migration of NSCLC cells induced by lipopolysaccharide（LPS）,but its mechanism is not clear.SAL has been shown to ameliorate metabolic inflammation in rodent diabetes by activating amp-activated Protein Kinase（AMPK）to inhibit NLRP3 inflammasome.However,whether NLRP3 inflammasome is regulated by SAL in NSCLC cells and how to determine its underlying molecular mechanisms still need to be explored.Objective: The purpose of this study was to investigate the role of SAL in LPS-induced proliferation and migration of human alveolar basal carcinoma epithelial cells（A549）,and the effects of SAL on production of Reactive Oxygen Species（ROS）and activation of NLRP3 inflammasome,and to explore the mechanism.Methods:1.The effect of SAL on LPS-induced human lung cancer A549 cell proliferation was detected by CCK-8 cell proliferation assay.2.The effect of SAL on LPS-induced migration of human lung cancer A549 cells was investigated by cell scratch assay.3.The expression levels of AMPK,NLRP3,Caspase-1 and IL-1β of SAL in LPS-induced human lung cancer A549 cells were detected by Western blot.4.To observe the effect of recombinant IL-1β protein on the above effects of SAL.5.Fluorescence probe was used to detect the effect of SAL on ROS level in human lung cancer A549 cells stimulated by LPS.6.To observe the effect of AMPK inhibitor（compound C,CC）on the above effects of SAL.Results:1.SAL inhibited LPS-induced proliferation of human lung cancer A549 cells.2.SAL inhibited LPS-induced migration of human lung cancer A549 cells.3.LPS inhibited AMPK activity and activated NLRP3 inflammasome,and SAL inhibited these changes.4.IL-1β could block the regulation of SAL on proliferation and migration of A549.5.SAL inhibited LPS-induced ROS over-production.6.CC could block the above effects of SAL.Conclusion:1.SAL inhibits the proliferation and migration of human lung cancer A549 cells in vitro.2.SAL inhibits the proliferation and migration of HUMAN lung cancer A549 cells through AMPK dependent inhibition of ROS-NLRP3 inflammasome signaling.