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Retinoic acid inhibits expression of TNF-α and iNOS in activated rat microglia

✍ Scribed by S. Thameem Dheen; Yan Jun; Zhou Yan; Samuel S.W. Tay; Eng Ang Ling

Publisher
John Wiley and Sons
Year
2005
Tongue
English
Weight
904 KB
Volume
50
Category
Article
ISSN
0894-1491

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✦ Synopsis

The release of proinflammatory mediators such as tumor necrosis factor-␣ (TNF-␣) and nitric oxide by microglia has been implicated in neurotoxicity in chronic neurodegenerative diseases such as Alzheimer's disease. As all-trans-retinoic acid (RA) has been reported to exert anti-inflammatory actions in various cell types, we have examined its effects on the expression of TNF-␣ and inducible nitric oxide synthase (iNOS) in microglia activated by ␤-amyloid peptide (A␤) and lipopolysaccharide (LPS). Exposure of primary cultures of rat microglial cells to A␤ or LPS stimulated the mRNA expression level of TNF-␣ (6 -116-fold) and iNOS (8 -500-fold) significantly. RA acted in a dose-dependent manner (0.1-10 M) by attenuating both TNF-␣ (29 -97%) and iNOS (61-96%) mRNA expression in microglia exposed to A␤ or LPS. RA-induced inhibition of TNF-␣ and iNOS mRNA expression in activated microglia was accompanied by the concomitant reduction in release of iNOS and TNF-␣ proteins as revealed by nitrite assay and ELISA, respectively. The anti-inflammatory effects of RA were correlated with the enhanced expression of retinoic acid receptor-␤, and transforming growth factor-␤1 as well as the inhibition of NF-B translocation. These results suggest that RA may inhibit the neurotoxic effect of activated microglia by suppressing the production of inflammatory cytokines and cytotoxic molecules.

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