Imai Yumi, Nakashima Yuya, Kanno Toshihiro
Department of Research and Development, Chlorella Industry Co., Ltd., Hisatomi 1343, Chikugo, Fukuoka 833-0056, Japan.
Evid Based Complement Alternat Med. 2022 Nov 1;2022:8789903. doi: 10.1155/2022/8789903. eCollection 2022.
Advanced glycation end products (AGEs) are formed via a nonenzymatic glycosylation reaction called glycation. The formation and accumulation of AGEs increases in skin with age, contributing to the appearance of facial wrinkles and loss of skin elasticity. Therefore, inhibition of AGEs may delay skin aging. The microalgae has been used as a health food supplement for many years and contains carotenoids and vitamins that have antioxidant and anti-inflammatory effects. The aim of this study was to investigate whether extract also has antiglycation activity. Antiglycation activity was measured using fluorescent AGEs, N-(carboxymethyl) lysine (CML), and N-(carboxymethyl) arginine (CMA) from glycated bovine serum albumin and type I collagen . A gel with a dermis-like structure consisting of collagen and a live fibroblast cell line was glycated with glyoxal. The content of fluorescent AGE, CML, and CMA, and the gel contraction activity were measured. In addition, to investigate the level of inflammation induced by the glycation of the collagen gel, the expression level of the receptor for AGEs and interleukin-8 were examined. Fat-soluble extract suppressed the formation of fluorescent AGEs, CML, and CMA in both models. These results indicated that extract directly inhibited AGE formation. The collagen gel contracted over time during culturing, whereas contraction was inhibited in the glyoxal-treated collagen gel. extract remarkably attenuated the glyoxal-induced gel contraction. Moreover, extract substantially decreased the fluorescent AGEs, CML, and CMA in the collagen gels with glyoxal. Glyoxal exposure increased the expression levels of interleukin-8 and receptor for AGE proteins in collagen gels, while extract inhibited this increase. This study showed that fat-soluble extract has a direct inhibitory effect on AGEs and decreases receptor expression for AGE-mediated inflammation by reducing AGEs. may delay skin aging by inhibiting the formation and accumulation of AGEs.
晚期糖基化终末产物（AGEs）是通过一种称为糖基化的非酶糖基化反应形成的。随着年龄的增长，皮肤中AGEs的形成和积累会增加，导致面部皱纹的出现和皮肤弹性的丧失。因此，抑制AGEs可能会延缓皮肤衰老。微藻作为一种保健食品补充剂已经使用多年，含有具有抗氧化和抗炎作用的类胡萝卜素和维生素。本研究的目的是调查[提取物名称]提取物是否也具有抗糖基化活性。使用来自糖化牛血清白蛋白和I型胶原蛋白的荧光AGEs、N-（羧甲基）赖氨酸（CML）和N-（羧甲基）精氨酸（CMA）来测量抗糖基化活性。用乙二醛使由胶原蛋白和活的成纤维细胞系组成的具有真皮样结构的凝胶糖化。测量荧光AGE、CML和CMA的含量以及凝胶收缩活性。此外，为了研究胶原蛋白凝胶糖化诱导的炎症水平，检测了AGEs受体和白细胞介素-8的表达水平。脂溶性提取物在两种模型中均抑制了荧光AGEs、CML和CMA的形成。这些结果表明[提取物名称]提取物直接抑制了AGE的形成。在培养过程中，胶原蛋白凝胶会随着时间的推移而收缩，而在乙二醛处理的胶原蛋白凝胶中收缩受到抑制。[提取物名称]提取物显著减弱了乙二醛诱导的凝胶收缩。此外，[提取物名称]提取物显著降低了含有乙二醛的胶原蛋白凝胶中的荧光AGEs、CML和CMA。乙二醛暴露增加了胶原蛋白凝胶中白细胞介素-8和AGE蛋白受体的表达水平，而[提取物名称]提取物抑制了这种增加。本研究表明，脂溶性提取物对AGEs有直接抑制作用，并通过减少AGEs来降低AGE介导的炎症的受体表达。[提取物名称]可能通过抑制AGEs的形成和积累来延缓皮肤衰老。
