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Original Research Article | OPEN ACCESS

Carum carvi Linn (Umbelliferae) attenuates lipopolysaccharide-induced neuroinflammatory responses via regulation of NF-KB signaling in BV-2 microglia

Spandana Rajendra Kopalli, Sushruta Koppula

College of Biomedical and Health Science, Konkuk University, Chungju-Si, Chungbuk Do, 380-701, Republic of Korea;

For correspondence:-  Sushruta Koppula   Email: sushrutak@gmail.com   Tel:+82438403609

Received: 25 March 2015        Accepted: 22 May 2015        Published: 29 June 2015

Citation: Kopalli SR, Koppula S. Carum carvi Linn (Umbelliferae) attenuates lipopolysaccharide-induced neuroinflammatory responses via regulation of NF-KB signaling in BV-2 microglia. Trop J Pharm Res 2015; 14(6):1041-1047 doi: 10.4314/tjpr.v14i6.15

© 2015 The authors.
This is an Open Access article that uses a funding model which does not charge readers or their institutions for access and distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0) and the Budapest Open Access Initiative (http://www.budapestopenaccessinitiative.org/read), which permit unrestricted use, distribution, and reproduction in any medium, provided the original work is properly credited..

Abstract

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, 5- diphenyl-tetrazolium 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 microglia-mediated neuroinflammation.

Keywords: Carum carvi, Anti-oxidant, Neuroinflammation, Microglia, Nitric oxide, Interleukin

Impact Factor
Thompson Reuters (ISI): 0.523 (2021)
H-5 index (Google Scholar): 39 (2021)

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