Yugang Jiang1, Kai Huang2, Xixia Lin2, Qinchang Chen2, Shaoyan Lin3, Xiaomin Feng4, Chaohui Zhen2, Min Huang2, Shenming Wang5. 1. Division of General Surgery of Shandong Provincial Hospital affiliated to Shandong University, Shandong, China sysumed2016@126.com wangshenming@21cn.com. 2. Division of Vascular and Thyroid Surgery in Sun Yat-sen Memorial Hospital of Sun Yat-sen University, Guangzhou, China. 3. National Cancer Center/Cancer Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, China. 4. Division of Vascular Surgery in the First Affiliated Hospital of Sun Yat-sen University, China. 5. Division of Vascular Surgery in the First Affiliated Hospital of Sun Yat-sen University, China sysumed2016@126.com wangshenming@21cn.com.
Abstract
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.
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 NLRP3inflammation activation by reducing IL-1β secretion from macrophages, which could be an important therapeutic target in atherosclerosis.
Authors: Juan M Suárez-Rivero; Carmen J Pastor-Maldonado; Suleva Povea-Cabello; Mónica Álvarez-Córdoba; Irene Villalón-García; Marta Talaverón-Rey; Alejandra Suárez-Carrillo; Manuel Munuera-Cabeza; José A Sánchez-Alcázar Journal: Biomedicines Date: 2021-03-05