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首页> 外文期刊>Natural product communications >Inhibition of the MAPK Signaling Pathway by Red Rice Extract in UVB-irradiated Human Skin Fibroblasts
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Inhibition of the MAPK Signaling Pathway by Red Rice Extract in UVB-irradiated Human Skin Fibroblasts

机译:红米提取物对紫外线照射的人皮肤成纤维细胞中MAPK信号通路的抑制作用

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Red rice has demonstrated several biological properties including anti-oxidant and anti-inflammation properties. However, the anti-photoaging activity has not yet been investigated. The aim of this study relates to the photo-protective effects of red rice extract (RRE) on UVB-induced skin aging. RRE was prepared and the active compounds and anti-oxidant activity were determined. The cytotoxicity of fibroblasts and secretions of IL-6 and IL-8 were evaluated. The effects of RRE on collagen and hyaluronic acid (HA) synthesis from fibroblasts were evaluated. Then, the collagenase and MMP-2 activity was determined. The effect of RRE on UV-induced MMP-1, nuclear factor kappa B (NF-kappa B), activator protein-I (AP-1) and phosphorylation of MAPK protein expression was determined by western blot analysis. The RRE exerted a free radical scavenging property. RRE significantly increased collagen and HA synthesis in UVB-irradiated human fibroblasts. Moreover, RRE significantly inhibited UVB induced MMP-1 expression, MMP-2 and collagenase activity. Upon UVB irradiation, mitogen activated protein kinases (MAPKs) is activated and this pathway stimulates the expression of interleukin-6 and-8 (IL-6 and-8). Our results show that RRE decreases UVB-induced IL-6 and-8 production and the phosphorylation of c-Jun NH2-terminal kinase (JNK) and the p38 MAPK signaling process. In addition, RRE reduced UVB-induced activation of NF-kappa B and AP-1. RRE could suppress UV-induced inflammation and skin aging via the inhibition of the MAPK signaling pathway leading to the decrease of NF-kappa B and AP-1 activation resulting in a decrease in ECM degradation and an increase in ECM synthesis.
机译:红米已显示出多种生物特性,包括抗氧化剂和抗发炎特性。然而,尚未研究抗光老化活性。这项研究的目的涉及红米提取物(RRE)对UVB诱导的皮肤衰老的光保护作用。制备了RRE,并测定了活性化合物和抗氧化活性。评价成纤维细胞的细胞毒性以及IL-6和IL-8的分泌。评估了RRE对成纤维细胞合成胶原和透明质酸(HA)的影响。然后,测定胶原酶和MMP-2活性。通过蛋白质印迹分析确定RRE对紫外线诱导的MMP-1,核因子κB(NF-κB),激活蛋白-1(AP-1)和MAPK蛋白表达的磷酸化的影响。 RRE具有自由基清除性能。 RRE显着增加了UVB辐射的人类成纤维细胞中的胶原蛋白和HA合成。此外,RRE显着抑制UVB诱导的MMP-1表达,MMP-2和胶原酶活性。在UVB照射下,促分裂原激活的蛋白激酶(MAPK)被激活,并且该途径刺激白介素6和8(IL-6和8)的表达。我们的结果表明,RRE降低了UVB诱导的IL-6和8的产生以及c-Jun NH2末端激酶(JNK)的磷酸化和p38 MAPK信号传导过程。此外,RRE减少了UVB诱导的NF-κB和AP-1的活化。 RRE可以通过抑制MAPK信号通路来抑制UV诱导的炎症和皮肤衰老,从而导致NF-κB和AP-1激活减少,从而导致ECM降解减少和ECM合成增加。

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