Shikonin Isolated from Lithospermum erythrorhizon Downregulates Proinflammatory Mediators in Lipopolysaccharide-Stimulated BV2 Microglial Cells by Suppressing Crosstalk between Reactive Oxygen Species and NF-kappaB
Biomolecules & Therapeutics
;
: 110-118, 2015.
Article
in English
| WPRIM
| ID: wpr-104385
ABSTRACT
According to the expansion of lifespan, neuronal disorder based on inflammation has been social problem. Therefore, we isolated shikonin from Lithospermum erythrorhizon and evaluated anti-inflammatory effects of shikonin in lipopolysaccharide (LSP)-stimulated BV2 microglial cells. Shikonin dose-dependently inhibits the expression of the proinflammatory mediators, nitric oxide (NO), prostaglandin E2 (PGE2), and tumor necrosis factor-alpha (TNF-alpha) as well as their main regulatory genes and products such as inducible NO synthase (iNOS), cyclooxygenase-2 (COX-2), and TNF-alpha in LPS-stimulated BV2 microglial cells. Additionally, shikonin suppressed the LPS-induced DNA-binding activity of nuclear factor-kappaB (NF-kappaB) to regulate the key regulatory genes of the proinflammatory mediators, such as iNOS, COX-2, and TNF-alpha, accompanied with downregulation of reactive oxygen species (ROS) generation. The results indicate that shikonin may downregulate the expression of proinflammatory genes involved in the synthesis of NO, PGE2, and TNF-alpha in LPS-treated BV2 microglial cells by suppressing ROS and NF-kappaB. Taken together, our results revealed that shikonin exerts downregulation of proinflammatory mediators by interference the ROS and NF-kappaB signaling pathway.
Full text:
Available
Index:
WPRIM (Western Pacific)
Main subject:
Social Problems
/
Dinoprostone
/
Down-Regulation
/
Genes, Regulator
/
NF-kappa B
/
Tumor Necrosis Factor-alpha
/
Reactive Oxygen Species
/
Nitric Oxide Synthase
/
Lithospermum
/
Cyclooxygenase 2
Language:
English
Journal:
Biomolecules & Therapeutics
Year:
2015
Type:
Article
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