Abstract:Objective: To observe the effect of ursolic acid (UA) on the biological activity of A549 cells derived from human pulmonary epithelial cells under lipopolysaccharide (LPS) and its potential mechanism. Methods: The CCK-8 method was used to detect the effect of UA (10, 50, 100, 150 and 200 μg/mL) at different concentrations on the proliferation of A549 cells. In addition, the effect of 10 ug/mL UA on the proliferation of A549 cells at different time points was also detected. The qPCR was used to detect the mRNA expression of interleukin (IL) -1β, IL-6 and tumor necrosis factor-α (TNF-α) in A549 cells under LPS. The effect of UA on the expression of IL-1β in A549 cells under LPS was detected by ELISA. Results: UA was able to significantly inhibit the activity of A549 cells. Results of CCK-8 showed that 10 μg/mL UA was able to significantly inhibit the activity of A549 cells after 24 hours of UA treatment (P<0.05). In addition, UA was able to significantly inhibit the mRNA expression of TNF-α, IL-1β and IL-6 induced by LPS (P<0.05). Among them, the inhibition effect of LPS-induced IL-1β was the most obvious. Results of ELISA showed that UA to inhibit inflammation was not influenced by ERK and JNK signaling pathway inhibitors, but p38 signaling pathway inhibitors was able to significantly reverse the inhibitory effect of UA on LPS-induced IL-1β (P<0.05). However, p38 signal pathway activator was able to reverse the inhibition effect (P<0.05). Conclusion: UA can inhibit the LPS-induced IL-1β and can exerts function through p38 pathway.
