KMID : 0606920150230020110
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Biomolecules & Therapeutics 2015 Volume.23 No. 2 p.110 ~ p.118
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Shikonin Isolated from Lithospermum erythrorhizon Downregulates Proinflammatory Mediators in Lipopolysaccharide-Stimulated BV2 Microglial Cells by Suppressing Crosstalk between Reactive Oxygen Species and NF-¥êB
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Prasad Rajapaksha Gedara
Choi Yung-Hyun Kim Gi-Young
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Abstract
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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-¥á (TNF-¥á) as well as their main regulatory genes and products such as inducible NO synthase (iNOS), cyclooxygenase-2 (COX-2), and TNF-¥á in LPS-stimulated BV2 microglial cells. Additionally, shikonin suppressed the LPS-induced DNA-binding activity of nuclear factor-¥êB (NF-¥êB) to regulate the key regulatory genes of the proinflammatory mediators, such as iNOS, COX-2, and TNF-¥á, 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-¥á in LPS-treated BV2 microglial cells by suppressing ROS and NF-¥êB. Taken together, our results revealed that shikonin exerts downregulation of proinflammatory mediators by interference the ROS and NF-¥êB signaling pathway.
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KEYWORD
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Shikonin, Proinflammatory mediators, Reactive oxygen species, Nuclear factor-¥êB
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