Purpose:
To investigate the anti
-
neuroinflammatory properties of
Carum carvi
Linn. (CCE,
Umbelliferae) aqueous extract in stimulate
d 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 enzym
e
-
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.
