{"title":"In Vivo Study on the Effect of Tetrahydropalmatine on the Activation of NLRP3 Inflammasome in BV-2 Cells","authors":"Mingjuan Zhang, Xiajun Yi, Qingying Zhan, Li Huang, Yadong Xiao, Jihui Zhong","doi":"10.1166/jbt.2024.3353","DOIUrl":null,"url":null,"abstract":"Background: The paper aimed to explore the effect of Tetrahydropalmatine on the activation of NLRP3 inflammasomes in BV-2 cells and its mechanism in vitro. Material and methods: ELISA determine the IL-1β and IL-18 in the BV-2 cell culture medium of each\n group. WB was employed to detect NLRP3 inflammasome-related components including NLRP3, ASC, NEK7 and Caspase-1, as well as p-NF-κB, NF-κB, p-Iκ-Bα and Iκ-Bα in cell lysates of each group. The effects of Tetrahydropalmatine\n on NLRP3 inflammasome activation and NF-κB signaling pathway were analyzed. Immunofluorescence labeling method was used to detect the expressions of NLRP3 in BV-2 cells in each group. Mito-tracker Red labeled mitochondrial confocal microscope was employed to observe and evaluate\n mitochondrial damage. Fluorescent probe DCFH-DA was used to label cells. Flow cytometry technology was applied to detect ROS production and evaluate the effect of Tetrahydropalmatine on ROS production. Results: After Tetrahydropalmatine treatment, p-NF-κB/NF-κB\n and p-Iκ-Bα/Iκ-Bα were significantly lower than that in the model group. Tetrahydropalmatine can inhibit the production of ROS and improve the mitochondrial membrane potential. Conclusion: Tetrahydropalmatine can mitigate mitochondrial\n damage, reduce ROS production, and inhibit the NF-κB signaling pathway, thereby inhibiting the activation of NLRP3 inflammasomes in BV-2 cells.","PeriodicalId":15300,"journal":{"name":"Journal of Biomaterials and Tissue Engineering","volume":"13 6","pages":""},"PeriodicalIF":0.1000,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Journal of Biomaterials and Tissue Engineering","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.1166/jbt.2024.3353","RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 0
Abstract
Background: The paper aimed to explore the effect of Tetrahydropalmatine on the activation of NLRP3 inflammasomes in BV-2 cells and its mechanism in vitro. Material and methods: ELISA determine the IL-1β and IL-18 in the BV-2 cell culture medium of each
group. WB was employed to detect NLRP3 inflammasome-related components including NLRP3, ASC, NEK7 and Caspase-1, as well as p-NF-κB, NF-κB, p-Iκ-Bα and Iκ-Bα in cell lysates of each group. The effects of Tetrahydropalmatine
on NLRP3 inflammasome activation and NF-κB signaling pathway were analyzed. Immunofluorescence labeling method was used to detect the expressions of NLRP3 in BV-2 cells in each group. Mito-tracker Red labeled mitochondrial confocal microscope was employed to observe and evaluate
mitochondrial damage. Fluorescent probe DCFH-DA was used to label cells. Flow cytometry technology was applied to detect ROS production and evaluate the effect of Tetrahydropalmatine on ROS production. Results: After Tetrahydropalmatine treatment, p-NF-κB/NF-κB
and p-Iκ-Bα/Iκ-Bα were significantly lower than that in the model group. Tetrahydropalmatine can inhibit the production of ROS and improve the mitochondrial membrane potential. Conclusion: Tetrahydropalmatine can mitigate mitochondrial
damage, reduce ROS production, and inhibit the NF-κB signaling pathway, thereby inhibiting the activation of NLRP3 inflammasomes in BV-2 cells.