AI Article Synopsis
- Glycosidic forms of flavonoids, like luteolin-7-O-glucoside, may be partially absorbed without needing to be hydrolyzed, and both forms of luteolin show potential for antioxidative activity.
- Both luteolin and luteolin-7-O-glucoside effectively induced the expression of heme oxygenase-1 (HO-1), an enzyme associated with antioxidative effects, likely through the activation of Nrf2 and specific signaling pathways (p38 and JNK).
- These compounds were shown to reduce oxidative damage in cells by enhancing HO-1 activity, confirming their role in fighting oxidative stress through targeted molecular mechanisms.
Article Abstract
It has been understood that glycosidic forms of flavonoids were hydrolyzed by gut bacteria and absorbed as aglycones. However, several reports suggested that glycosides were partly absorbed without hydrolysis and remained biologically active. In this study, we evaluated the antioxidative potential of luteolin and luteolin-7-O-glucoside, glycosidic form of luteolin, against the oxidative damage and compared their antioxidative mechanisms in RAW 264.7 cells. Heme oxygenase-1 (HO-1), one of the phase II enzymes showing an antioxidative activity, was potently induced by luteolin and luteolin-7-O-glucoside treatment, which was in accordance with the translocated nuclear factor-erythroid 2 p45-related factor 2 (Nrf2) into nucleus. Moreover, luteolin and the luteolin-7-O-glucoside activated HO-1 expression by p38 and c-Jun NH2-terminal kinase (JNK) regulation. In order to identify the antioxidation potential by HO-1, tert-butyl hydroperoxide (t-BHP)-induced oxidative damage was applied and ameliorated by luteolin and the luteolin-7-O-glucoside treatment in a dose dependent manner, which was confirmed by HO-1 selective inhibitor and inducer, tin protoporphyrin (SnPP) and cobalt protoporphyrin (CoPP), respectively. Consequently, luteolin and luteolin-7-O-glucoside potently strengthen the HO-1-mediated antioxidative potential through the modulation of the Nrf2/MAPK signaling pathways.
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| http://dx.doi.org/10.1016/j.fct.2013.12.017 | DOI Listing |
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