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Updated: Jan 22, 2026

Author Spotlight: Induced Microglia-Like Cell Technology to Shed Light on the Role of Microglial Dysfunction in Neuropsychiatric Disorders
Published on: September 6, 2024
Naringin inhibits lipopolysaccharide-induced activation of microglia cells
Jie Bai1, Siyuan Li1, Gang Wu1
1Department of Anesthesiology, the Second Affiliated Hospital of Xi'an Jiaotong University, 710004, Xi'an, Shaanxi, China.
Abstract:
The purpose of this study was to investigate the effect of naringin on lipopolysaccharide (LPS)-induced activation of BV2 microglia and inflammatory factor release, and the mechanism involved. Different concentrations of naringin were used to pretreat BV2 cells for 30 min, after which they were stimulated with 100 ng/mL LPS for different durations. The levels of NO, IL-1β and TNF-α in the cell culture medium was determined with ELISA and Griess method. The mRNA expressions of IL-1β and TNF-α was determined with RT-PCR. Changes in ERK and p65/NF-κB signaling pathway proteins were assayed with Western blotting. After 12 h stimulation of BV2 cells with LPS, the levels of IL-1β and TNF-α in the cell culture medium were significantly increased, but naringin had no significant effect on these inflammatory factors. In the cells pretreated with naringin, LPS stimulated the activation of microglia to produce IL-1β and TNF-α in a dose-dependent manner. Naringin inhibited LPS-induced release of IL-1β, to a certain extent. The TNF-α gene was overexpressed. In addition, LPS stimulated a dose-dependent decrease in NO production by BV2 after pretreatment with different concentrations of naringin. Naringin pretreatment of cells significantly inhibited the activation of p65/NF-κB in a concentration-dependent manner. In BV2 microglia, naringin inhibits LPO-induced production of NO and inflammatory factors, through a mechanism involving inhibition of activation of the p65/NF-κB signaling pathway.
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