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Effects of the Aqueous Extract of Rehmanniae Radix Preparata on Lipopolysaccharide-induced Expressions of Cyclooxygenase-2 and Inducible Nitric Oxide Synthase in Mouse BV2 Microglial Cells  

Jung, Chang-Young (Department of Physiology, College of Oriental Medicine, Kyungwon University)
Sung, Yun-Hee (Department of Physiology, College of Medicine, Kyung Hee University)
Kim, Sung-Eun (Department of Physiology, College of Medicine, Kyung Hee University)
Kim, Chang-Ju (Department of Physiology, College of Medicine, Kyung Hee University)
Han, Seung-Ho (Department of Physiology, College of Medicine, Eulji University)
Lee, Choong-Yeol (Department of Physiology, College of Oriental Medicine, Kyungwon University)
Publication Information
Journal of Physiology & Pathology in Korean Medicine / v.20, no.4, 2006 , pp. 1051-1056 More about this Journal
Abstract
Rehmanniae radix preparata is the root of Rehmanniae glutinosa Liboschitz var. purpurea Makino which has been classified into Scrophulariaceae. Rehmanniae radix preparata has been used for the treatment of diabetes, for the relief of the pain, and for the anti-oxidative action. In this study, the effect of the aqueous extract of Rehmanniae radix preparata on lipopolysaccharide-induced inflammation was investigated by using 3-(4,5-dimethylthiazol- 2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay, reverse transcription-polymerase chain reaction (RT-PCR), Western blot, prostaglandin E2 immunoassay, and nitric oxide (NO) detection in mouse BV2 microglial cells. In the present results, the aqueous extract of Rehmanniae radix preparata suppressed prostaglandin E2 (PGE2) synthesis and nitric oxide production by inhibiting the lipopolysaccharide-stimulated expressions of cyclooxygenase-2 (COX-2) and inducible nitric oxide synthase (iNOS) mRNA and protein in mouse BV2 cells. These results show that Rehmanniae radix preparata exerts anti-inflammatory effect probably by suppressing of COX-2 and iNOS expressions.
Keywords
Rehmanniae radix preparata; lipopolysaccharide; cyclooxygenase-2; prostaglandin E2; nitric oxide;
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