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中国精品科技期刊2020
郭开恩,闫宫花,曾鑫,等. 复方胶原蛋白肽粉对皮肤慢性紫外线损伤小鼠的改善作用及机制研究[J]. 华体会体育,2023,44(15):401−409. doi: 10.13386/j.issn1002-0306.2022100294.
引用本文: 郭开恩,闫宫花,曾鑫,等. 复方胶原蛋白肽粉对皮肤慢性紫外线损伤小鼠的改善作用及机制研究[J]. 华体会体育,2023,44(15):401−409. doi: 10.13386/j.issn1002-0306.2022100294.
GUO Kaien, YAN Gonghua, ZENG Xin, et al. Compound Collagen Peptides Powder Improves Chronic Skin Damage Resulting from Ultraviolet Irradiation in Mice and the Mechanism[J]. Science and Technology of Food Industry, 2023, 44(15): 401−409. (in Chinese with English abstract). doi: 10.13386/j.issn1002-0306.2022100294.
Citation: GUO Kaien, YAN Gonghua, ZENG Xin, et al. Compound Collagen Peptides Powder Improves Chronic Skin Damage Resulting from Ultraviolet Irradiation in Mice and the Mechanism[J]. Science and Technology of Food Industry, 2023, 44(15): 401−409. (in Chinese with English abstract). doi: 10.13386/j.issn1002-0306.2022100294.

复方胶原蛋白肽粉对皮肤慢性紫外线损伤小鼠的改善作用及机制研究

Compound Collagen Peptides Powder Improves Chronic Skin Damage Resulting from Ultraviolet Irradiation in Mice and the Mechanism

  • 摘要: 目的:观察复方胶原蛋白肽粉对小鼠皮肤慢性紫外线损伤的改善作用,并探讨其作用机制。方法:ICR雌性小鼠随机分成正常组、模型组、复方胶原蛋白肽粉组、鱼胶原蛋白肽组。使用紫外光疗仪模拟日光照射小鼠背部皮肤建立皮肤慢性紫外线损伤模型。每周对小鼠皮肤表观进行评分,每3周拍照记录一次小鼠皮肤外观,9周后采用干燥法测定小鼠皮肤含水量;苏木精-伊红(HE)染色法观察小鼠皮肤组织病理形态学变化;采用FRAP法检测小鼠皮肤组织中总抗氧化能力(T-AOC)水平;酶联免疫吸附(ELISA)法检测皮肤组织中I型胶原蛋白(Col I)、弹性蛋白(ELN)、透明质酸(HA)、超氧化物歧化酶(SOD)、谷胱甘肽过氧化物酶(GSH-Px)、丙二醛(MDA) 、糖基化终末产物(AGEs)水平;采用蛋白免疫印迹法(Western blot)检测皮肤组织中转化生长因子β1(TGF-β1)、转化生长因子β受体2(TGF-βR2)、Smad2、Smad3、Smad7蛋白表达水平;采用实时荧光定量聚合酶链式反应(RT-qPCR)检测皮肤组织中TGF-β1TGF-βR2Smad2Smad3Smad7 mRNA表达水平。结果:与模型组比较,复方胶原蛋白肽粉组小鼠皮肤皱纹减少,无表皮损伤,宏观等级评分极显著降低(P<0.01),皮肤组织病变程度减轻;皮肤组织含水量极显著升高(P<0.01);皮肤组织T-AOC水平极显著升高(P<0.01);皮肤组织中Col I、ELN、HA、GSH-Px、SOD水平极显著升高(P<0.01),MDA、AGEs水平极显著降低(P<0.01);皮肤组织的TGF-β1、TGF-βR2、Smad2、Smad3蛋白及mRNA表达显著升高(P<0.05),Smad7蛋白及mRNA表达极显著降低(P<0.01)。结论:复方胶原蛋白肽粉可有效改善小鼠皮肤慢性紫外线损伤,其机制可能与减轻氧化应激反应,调控TGF-β1/Smads信号转导增加细胞外基质合成有关。

     

    Abstract: Objective: To study the effect and action mechanism of compound collagen peptides powder on chronic skin damage resulting from ultraviolet irradiation in mice. Methods: Female ICR mice were randomly divided into the following groups according to their weights: Normal, model, compound collagen peptides powder, fish collagen peptide. Mice in the model and treatment groups were irradiated on back skin using UV phototherapy apparatus to induce chronic skin damage. During the experiment, the skin appearance of mice was scored each week and photos were taken every 3 weeks. The skin water content was determined by drying method after 9 weeks. The histopathological changes of mice skin were observed using Hematoxylin-Eosin (HE) staining. The total antioxidant capacity (T-AOC) in skin was detected using fluorescene recovery after photobleaching (FRAP). The levels of type I collagen (Col I), elastin (ELN), hyaluronic acid (HA), superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), malondialdehyde (MDA) and advanced glycation end products (AGEs) in the skin were examined using ELISAs. RT-PCR and Western blot analyses were performed to determine the mRNA and protein expression of transforming growth factor β1 (TGF-β1), transforming growth factor β receptor 2 (TGF-βR2), Smad2, Smad3 and Smad7. Results: Compared to the model group, mice in the compound collagen peptides powder group had less wrinkles, no epidermal damage and the skin scores were significantly decreased (P<0.01). The lesions of skin were improved. The water content of skin and T-AOC were significantly increased (P<0.01). The levels of Col I, ELN, HA, GSH-Px, SOD in the skin were significantly increased (P<0.01), whereas MDA and AGEs were significantly decreased (P<0.01). In the skin, the mRNA and protein expression of TGF-β1, TGF-βR2, Smad2, Smad3 were increased (P<0.05), whereas Smad7 was significantly decreased (P<0.01). Conclusion: The compound collagen peptides powder improved the chronic skin damage caused by ultraviolet irradiation. The action mechanism seemed to be related to reduction of oxidative stress, regulation and control signal transduction of TGF-β1/Smads pathway for increasing extracellular matrix synthesis.

     

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