Ultraviolet B (UVB) irradiation is major causative factor in skin aging. The aim of the present study was to investigate the protective effect of a 50% ethanol extract from Nypa fruticans (NF50E) against UVB-induced skin aging. The results indicated that NF50E exerted potent antioxidant activity (IC₅₀ = 17.55 ± 1.63 and 10.78 ± 0.63 μg/mL for DPPH and ABTS-radical scavenging activity, respectively) in a dose-dependent manner. High-performance liquid chromatography revealed that pengxianencin A, protocatechuic acid, catechin, chlorogenic acid, epicatechin, and kaempferol were components of the extract. In addition, the extract exhibited elastase inhibitory activity (IC₅₀ = 17.96 ± 0.39 μg/mL). NF50E protected against UVB-induced HaCaT cell death and strongly suppressed UVB-stimulated cellular reactive oxygen species generation without cellular toxicity. Moreover, topical application of NF50E mitigated UVB-induced photoaging lesions including skin erythema and skin thickness in BALB/C mice. NF50E treatment inhibited UVB-induced collagen degradation as well as MMP-1 and IL-1β expressions and significantly stimulated SIRT1 expression. Furthermore, the extract treatment markedly suppressed the activation of NF-κB and AP-1 (p-c-Jun) by deactivating the p38 and JNK proteins. Taken together, current data suggest that NF50E exhibits potent antioxidant potential and protection against photoaging by attenuating MMP-1 activity and collagen degradation possibly through the downregulation of MAPK/NF-κB/AP-1 signaling and SIRT1 activation.

中文翻译：

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通过抑制MAPK / AP-1 / MMP-1信号传导来防止Nypa Fruticans对UVB诱导的光老化。

紫外线B（UVB）辐射是皮肤衰老的主要诱因。本研究的目的是研究50％的南番果乙醇提取物（NF50E）对UVB诱导的皮肤衰老的保护作用。结果表明，NF50E施加强大的抗氧化活性（IC ₅₀  = 17.55±1.63和10.78±0.63  μ克/ mL的DPPH和ABTS自由基清除活性，分别地）以剂量依赖的方式。高效液相色谱法显示，彭仙草素A，原儿茶酸，儿茶素，绿原酸，表儿茶素和山emp酚是提取物的成分。另外，该提取物显示出弹性蛋白酶的抑制活性（IC ₅₀  = 17.96±0.39  μg / mL）。NF50E可防止UVB诱导的HaCaT细胞死亡，并强烈抑制UVB刺激的细胞产生活性氧而没有细胞毒性。此外，局部应用NF50E可减轻UVB诱导的BALB / C小鼠的光老化损伤，包括皮肤红斑和皮肤厚度。NF50E处理抑制UVB诱导的胶原蛋白降解以及MMP-1和IL- 1β表达，并显着刺激SIRT1表达。此外，提取物处理明显抑制NF-的激活κB和AP-1（pc-Jun）使p38和JNK蛋白失活。总之，目前的数据表明，表现出NF50E强大的抗氧化电势和防止由可能通过MAPK / NF-的下调衰减MMP-1的活性和胶原降解光老化κ B / AP-1信号和SIRT1激活。