首页> 美国卫生研究院文献>Molecules >CopA3 Peptide Prevents Ultraviolet-Induced Inhibition of Type-I Procollagen and Induction of Matrix Metalloproteinase-1 in Human Skin Fibroblasts
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CopA3 Peptide Prevents Ultraviolet-Induced Inhibition of Type-I Procollagen and Induction of Matrix Metalloproteinase-1 in Human Skin Fibroblasts

机译:CopA3肽可预防紫外线诱导的人皮肤成纤维细胞对I型胶原蛋白的抑制和基质金属蛋白酶-1的诱导。

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摘要

Ultraviolet (UV) exposure is well-known to induce premature aging, which is mediated by matrix metalloproteinase-1 (MMP-1) activity. A 9-mer peptide, CopA3 (CopA3) was synthesized from a natural peptide, coprisin, which is isolated from the dung beetle Copris tripartitus. As part of our continuing search for novel bioactive natural products, CopA3 was investigated for its in vitro anti-skin photoaging activity. UV-induced inhibition of type-I procollagen and induction of MMP-1 were partially prevented in human skin fibroblasts by CopA3 peptide in a dose-dependent manner. At a concentration of 25 μM, CopA3 nearly completely inhibited MMP-1 expression. These results suggest that CopA3, an insect peptide, is a potential candidate for the prevention and treatment of skin aging.
机译:众所周知,紫外线(UV)会引起过早衰老,这是由基质金属蛋白酶1(MMP-1)活性介导的。 9肽肽CopA3(CopA3)是由天然肽coprisin合成的,coprisin是从甲虫Copris tripartitus分离的。作为我们不断寻找新型生物活性天然产物的一部分,对CopA3的体外抗皮肤光老化活性进行了研究。在人皮肤成纤维细胞中,CopA3肽以剂量依赖的方式部分阻止了UV诱导的I型胶原蛋白的抑制和MMP-1的诱导。在25μM的浓度下,CopA3几乎完全抑制了MMP-1的表达。这些结果表明,昆虫肽CopA3是预防和治疗皮肤衰老的潜在候选者。

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