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methoxyl/necrosis

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17-Methoxyl-7-hydroxy-benzene-furanchalcone (MHBFC), a monomer isolated from the root of Millettia pulchra (Benth.) Kurz var. Laxior (Dunn) Z. Wei (Papilionaceae), has been demonstrated to exhibit protective effects on myocardial ischemia/reperfusion (I/R) injury in rats. However, the mechanisms for

5-Methoxyl Aesculetin Abrogates Lipopolysaccharide-Induced Inflammation by Suppressing MAPK and AP-1 Pathways in RAW 264.7 Cells.

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For the first time, a pale amorphous coumarin derivative, 5-methoxyl aesculetin (MOA), was isolated from the dried bark of Fraxinus rhynchophylla Hance (Oleaceae). MOA modulates cytokine expression in lipopolysaccharide (LPS)-treated RAW 264.7 macrophages, but the precise mechanisms are still not
Organoselenium compounds display important antioxidant activity and many biological activities interesting from pharmacological point of view. The aim of this study was to evaluate the hepatoprotective effect of p-methoxyl-diphenyl diselenide, a disubstituted diaryl diselenide, on acute liver injury

The effect of 17-methoxyl-7-hydroxy-benzene-furanchalcone isolated from Millettia pulchra on myocardial ischemia in vitro and in vivo.

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The effect of 17-methoxyl-7-hydroxy-benzene-furanchalcone isolated from the roots of Millettia pulchra (Benth.) Kurz var. Laxior (Dunn) Z. Wei on rat myocardial ischemia has been investigated. An in vitro cardiocyte apoptosis model and an in vivo myocardial ischemia model were used to elucidate the

Cytoprotective effects of heme oxygenase-1 induction by 3-O-caffeoyl-1-methylquinic acid.

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The novel antioxidant 3-O-caffeoyl-one-methylquinic acid (MCGA3) is a methyl chlorogenic acid derivative isolated from bamboo leaves. MCGA3 scavenges reactive oxygen species (ROS) and inhibits lipid peroxidation and xanthine oxidase in vitro. In this study, we evaluated the cytoprotective effect of

Cardamonin, inhibits pro-inflammatory mediators in activated RAW 264.7 cells and whole blood.

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Some chalcones, such as hydroxychalcones have been reported previously to inhibit major pro-inflammatory mediators such as nitric oxide (NO), prostaglandin E(2) (PGE(2)), tumor necrosis factor-alpha (TNF-alpha) and reactive oxygen species production by suppressing inducible enzyme expression via

Oral repletion of iron induces free radical mediated alterations in the gastrointestinal tract of rat.

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Free radical mediated effects on the gastrointestinal (GI) tract were studied by supplementing 8 mg of iron orally for 15 days to groups of both control (C+) and iron deficient (D+) rats. They were compared with their respective unsupplemented groups C and D. Incorporation of 3H-thymidine into the
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