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Downregulation of pro-inflammatory mediators by a water Schisandra chinensis extract (Turcz.) Baill fruit in lipopolysaccharide-stimulated RAW 264.7 ma...

Date:2016/8/30 23:23:29

Downregulation of pro-inflammatory mediators by a water Schisandra chinensis extract (Turcz.) Baill fruit in 

lipopolysaccharide-stimulated RAW 264.7 ma...Schisandra chinensis extract has a long-standing history of medicinal 

use as a tonic, a sedative, an anti-tussive, and an anti-aging drug. Nevertheless, the antagonistic effects of 

Schisandra chinensis extract against lipopolysaccharide (LPS)-stimulated responses have not yet been studied. 


In this study, we investigated whether water Schisandra chinensis extract fruit(WESC) has the ability to 

attenuate the expression of pro-inflammatory mediators such as nitric oxide (NO), prostaglandin E2 (PGE2), and 

tumor necrosis factor-α (TNF-α) in LPS-stimulated RAW 264.7 macrophage cells. WESC inhibited the expression 

of LPS-induced pro-inflammatory mediators, namely, NO, PGE2, and TNF-α. Furthermore, gene expression of inducible 

NO synthase (iNOS), cyclooxygenase-2 (COX-2), and TNF-α was inhibited both at mRNA and protein synthesis levels, 

without any cytotoxic effect. Moreover, WESC significantly suppressed LPS-induced DNA-binding activity of NF-κB 

by inhibiting degradation of IκBα. It was found that pyrrolidine dithiocarbamate (PDTC), a specific NF-κB 

inhibitor, downregulates the expression of these pro-inflammatory genes to be closely regulated by NF-κB 

activity. Furthermore, we found that WESC retains dephosphorylation of Akt in response to LPS, and consequently 

suppressed the DNA-binding activity of NF-κB in RAW 264.7 macrophage cells. LY294002, a specific Akt inhibitor, 

attenuated LPS-induced pro-inflammatory gene expression via suppression of NF-κB activity. Taken together, 

our results indicate that WESC downregulates the expression of pro-inflammatory genes involved in the synthesis 

of NO, PGE2, and TNF-α in LPS-stimulated RAW 264.7 macrophage cells by suppressing Akt-dependent NF-κB activity.