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.

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