Abstract
In this study, we investigated the antioxidant activity and anti-photoaging properties of an extract of Flemingia macrophylla, a plant rich in isoflavonoid content. Pretreatment of fibroblasts with Flemingia macrophylla extract (FME) inhibited elastase activity, promoted the protein expression of type I procollagen, and attenuated the phosphorylation of mitogen-activated protein (MAP) kinase and the protein expression of matrix-metalloproteinase- (MMP-) 1, 3, and 9. The IC50 values were 2.1 μg/mL for DPPH radical scavenging ability, 366.8 μg/mL for superoxide anion scavenging ability, 178.9 μg/mL for hydrogen peroxide scavenging ability, and 230.9 μg/mL for hydroxyl radical scavenging ability. Also, exposure of erythrocytes to various concentrations of FME (50–500 μg/mL) resulted in a dose- and time-dependent inhibition of AAPH-induced hemolysis. In human fibroblasts, FME at 10 μg/mL was shown to be a potent scavenger of UV-induced reactive oxygen species (ROS). The antioxidant and anti-photoaging properties of FME make it an ideal anti-intrinsic aging and anti-photoaging agent.
Highlights
Overexposure to ultraviolet (UV) irradiation can result in edema, erythema, inflammation, hyperpigmentation, hyperplasia, and photoaging as well as DNA damage and mutations in skin [1]
We investigated the antioxidant activities of Flemingia macrophylla extract (FME) and its effects on protein expression of matrix metalloproteinases (MMPs), elastase, and type I procollagen in human dermal fibroblasts after exposure to UVB
Acetonitrile, methanol, dimethyl sulfoxide (DMSO), phosphoric acid, gallic acid, quercetin, aluminum chloride hexahydrate (AlCl3), potassium acetate (CH3 COOK), calcium chloride (CaCl2), propylene glycol (PG), DL-dithiothreitol, Folin-Ciocalteu reagent, 1,1-diphenyl-2picrylhydrazyl radical (DPPH), 2,2-azobis(2-methylproptuiorincamaciiddin(eT)BdAih)y, d2ro,7ch-dloircihdleor(oAfAluPoHre)s,cFineCdli2a,c2e-ttahtieo-(bDaCrbFi-DA),3-(2-pyridyl)-5,6-diphenyl-1,2,3-triazine-4,4-disulfonic acid sodium salt (Ferrozine), butanol, pyridine, sodium nitrite, trichloroacetic acid (TCA), and deoxyribose were purchased from Sigma-Aldrich Chemicals
Summary
Overexposure to ultraviolet (UV) irradiation can result in edema, erythema, inflammation, hyperpigmentation, hyperplasia, and photoaging as well as DNA damage and mutations in skin [1]. Studies have demonstrated that UVB-induced oxidative stress causes cell structure damage and affects the repair and transcription of DNA as well as the synthesis of proteins [4, 5]. UVB irradiation damages the antioxidant defense system, impairs signal transduction pathways in skin cells, and degrades extracellular matrix (ECM) proteins, including collagen, elastin, proteoglycans, and fibronectin [6, 7]. Genistin was reported to inhibit UV-induced DNA damage [15], and its aglycone, genistein, was shown to prevent skin damage in mice [16] and UVB-induced premature senescence in human fibroblasts [17]. We investigated the antioxidant activities of FME and its effects on protein expression of MMPs, elastase, and type I procollagen in human dermal fibroblasts after exposure to UVB
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