Biomol Ther.
2013 Mar;21(2):146-152.
A Methanol Extract of Adansonia digitata L. Leaves Inhibits Pro-Inflammatory iNOS Possibly via the Inhibition of NF-kappaB Activation
- Affiliations
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- 1Food Science and Nutrition Program, Addis Ababa University, Ethiopia.
- 2Department of SCH-BioPharm Human Resources Development Center, Soonchunhyang University, Asan 336-646, Republic of Korea. kwnam1@sch.ac.kr
- 3Department of Chemistry, Soonchunhyang University, Asan 336-646, Republic of Korea.
- 4Department of Food Science and Nutrition, Soonchunhyang University, Asan 336-646, Republic of Korea. hskim1@sch.ac.kr
Abstract
- This study examined the total polyphenol content of eight wild edible plants from Ethiopia and their effect on NO production in Raw264.7 cells. Owing to its relatively high polyphenol concentration and inhibition of NO production, the methanol extract of Adansonia digitata L. leaf (MEAD) was subjected to detailed evaluation of its antioxidant and anti-inflammatory effects. Antioxidant effects were assessed by measuring free-radical-scavenging activity using 1,1-diphenyl-2-picrylhydrazyl (DPPH) and oxygen-radical-absorbance capacity (ORAC) assays, while anti-inflammatory effects were assessed by measuring inducible nitric oxide synthase (iNOS) expression in lipopolysaccharide (LPS)-stimulated RAW264.7 cells. In the ORAC assay, MEAD was 10.2 times more potent than vitamin C at eliminating peroxyl radicals. In DPPH assay, MEAD also showed a strong ROS scavenging effect. MEAD significantly inhibited iNOS activity (IC50=28.6 microg/ml) of LPS-stimulated Raw264.7 cells. We also investigated the relationship between iNOS expression and nuclear factor kappa B (NF-kappaB) activation. MEAD inhibited IkappaBa degradation and NF-kappaB translocation from the cytosol to the nucleus in LPS-induced RAW264.7 cells without significant cytotoxic effects, as confirmed by MTT assay. These results suggest that MEAD inhibits anti-inflammatory iNOS expression, which might be related to the elimination of peroxyl radicals and thus the inhibition of IkappaBa-mediated NF-kappaB signal transduction.