Berberine Attenuates NLRP3 Inflammasome Activation in Macrophages to Reduce the Secretion of Interleukin-1β

Objectives: The purpose of this study is to evaluate whether Berberine can suppress the inflammatory response in atherosclerosis lesions and its potential associated signaling pathways and mechanism of action.

Methods: We isolated human peripheral blood mononuclear cells. After co-culturing them with ox-LDL stimulated cells, ROS was measured by its fluorescence intensity and NADPH oxidase activity was detected by the OD value from the spectrophotometer. Human peripheral blood mononuclear cells were then pretreated with different concentrations of berberine after treatment with NLRP3 activator ATP. Western blot was used to measure the releas of IL-1β. We also used confocal microscopy to detect the nuclear import of NF-kB in macrophages.

Results: In this study we observed that berberine suppressed IL-1β secretion that was induced by the activation of the NLRP3 inflammasome in macrophages. In addition, we demonstrated that berberine may possibly reduce reactive oxygen species (ROS)-dependent NLRP3 inflammasome activation. Moreover, Berberine inhibited the expression of pro-IL-1β through inhibition of the nuclear factor κb (NF-κB) pathway, which prevented the priming IL-1β secretion.

Conclusion: Our results suggest that berberine alleviates NLRP3 inflammation activation by reducing IL-1β secretion from macrophages, which could be an important therapeutic target in atherosclerosis.