Carum carvi Linn (Umbelliferae) Attenuates Lipopolysaccharide-Induced Neuroinflammatory Responses via Regulation of NF-κB Signaling in BV-2 Microglia

Purpose: To investigate the anti-neuroinflammatory properties of Carum carvi Linn. (CCE, Umbelliferae) aqueous extract in stimulated BV-2 microglial cells and explore its underlying mechanisms. Methods: Cell viability assessment was performed by 3-(4, 5-dimethylthiazol-2-yl)-2, 5diphenyltetrazolium bromide (MTT) assay. Lipopolysaccharide (LPS) was used to activate BV-2 microglia. Nitric oxide (NO) levels were measured using Griess assay. Inducible NO synthase (iNOS) and cyclooxygenase (COX) levels were evaluated by Western blot analysis. Interleukin-6 (IL-6) and tumor necrosis factor-alpha (TNF-α) production were evaluated by enzyme-linked immunosorbent assay (ELISA). Results: CCE alone did not exhibit any signs of cytotoxicity to BV-2 cells up to 200 μg/ml concentration. The LPS-activated excessive release of NO in BV-2 cells was significantly inhibited by CCE (p < 0.001 at 100 μg/mL). CCE also inhibited the production of inflammatory mediators such as iNOS, COX-2, IL-6 and TNF-α (p < 0.05, p < 0.01 and p < 0.001 at 25, 50 and 100 μg/mL, respectively). Further mechanistic study revealed that CCE acts by regulation of nuclear factor kappa-B (NF-κB) signaling pathway in LPS-stimulated BV-2 microglial cells. Conclusion: The results reveal that CCE exhibited its anti-neuroinflammatory effects via regulation of NF-κB signaling. This can be developed as a potential therapeutic target in ameliorating microgliamediated neuroinflammation.