In Vivo Study on the Effect of Tetrahydropalmatine on the Activation of NLRP3 Inflammasome in BV-2 Cells

IF 0.1 4区 医学
Mingjuan Zhang, Xiajun Yi, Qingying Zhan, Li Huang, Yadong Xiao, Jihui Zhong
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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.
四氢巴马汀对 BV-2 细胞中 NLRP3 炎症小体激活作用的体内研究
研究背景本文旨在探讨四氢巴马汀对 BV-2 细胞中 NLRP3 炎症小体活化的影响及其体外机制。材料与方法ELISA 检测各组 BV-2 细胞培养液中的 IL-1β 和 IL-18。WB检测各组细胞裂解液中NLRP3炎症体相关成分,包括NLRP3、ASC、NEK7和Caspase-1,以及p-NF-κB、NF-κB、p-Iκ-Bα和Iκ-Bα。分析四氢巴马汀对 NLRP3 炎性体活化和 NF-κB 信号通路的影响。免疫荧光标记法检测各组 BV-2 细胞中 NLRP3 的表达。采用线粒体追踪红标记共聚焦显微镜观察和评估线粒体损伤。荧光探针 DCFH-DA 用于标记细胞。应用流式细胞术检测 ROS 的产生,并评估四氢巴马汀对 ROS 产生的影响。结果四氢巴马汀治疗后,p-NF-κB/NF-κB和p-Iκ-Bα/Iκ-Bα明显低于模型组。四氢巴马汀可抑制 ROS 的产生,提高线粒体膜电位。结论四氢巴马汀可减轻线粒体损伤,减少 ROS 的产生,抑制 NF-κB 信号通路,从而抑制 BV-2 细胞中 NLRP3 炎性体的活化。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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