Naringenin Ameliorates LPS-Induced Neuroinflammation Through NF-κB Signaling in Human Microglia and Protects Neuronal Cells

Background: Engagement of the NF-κB signaling pathway is crucial for controlling im-mune and inflammatory gene expression within the central nervous system (CNS). Naringenin, a flavonoid derived from citrus fruits, is known for its anti-inflammatory and antioxidant effects; however, its impact on LPS-induced neuroinflammation in HMC3 (human microglial) and SH-SY5Y (neuronal) cell lines has not been thoroughly studied. Objectives: To ascertain the neuroprotective role of Naringenin on LPS-induced neuroin-flammation in microglia and neuronal cell lines with focus on modulation of NF-κB sig-naling pathway. Methods: LPS treatment was given to HMC3 cells to induce an inflam-matory response and secretome of HMC3 cells to SH-SY5Y cells with the administration of Naringenin. The cell viability assay, ROS levels, Western blotting, immunocytochemis-try were employed to quantify and localize NF-κB and pro-inflammatory cytokines (TNF-α, IL-6, IL-1β). Nuclear and cytosolic fractions of NF-κB were analyzed to screen its activation and translocation. Results: Naringenin treatment led to a dose-dependent de-crease in LPS-induced reactive oxygen species (ROS) production. It significantly reduced the expression of pro-inflammatory cytokines and inhibited NF-κB activation in HMC3 cells. The nuclear translocation of NF-κB was notably diminished after treatment, as demonstrated by both western blot and immunocytochemistry. These results suggest that Naringenin exerts an anti-inflammatory effect by suppressing the NF-κB signaling path-way. Conclusion: The findings suggest the potential therapeutic role of Naringenin using in vitro models in mitigating neuroinflammation through modulation of NF-κB signaling pathway