研究报告

灵芝孢子粉提取物延缓皮肤衰老作用研究

  • 刘春媛 ,
  • 刘振华 ,
  • 陈云霞 ,
  • 何婕 ,
  • 薛圣然 ,
  • 张心怡 ,
  • 郑君 ,
  • 苏宁
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  • 1(中国检验检疫科学研究院,北京,100176)
    2(中检科(北京)化妆品技术有限公司,北京,100176)
硕士,助理研究员(苏宁副研究员为通信作者,E-mail:sun@caiq.org.cn)

收稿日期: 2022-05-18

  修回日期: 2022-06-21

  网络出版日期: 2023-04-28

基金资助

中国检验检疫科学研究院基本科研业务费项目(2020JK040)

Anti-skin aging effect of Ganoderma lucidum spore extract

  • LIU Chunyuan ,
  • LIU Zhenhua ,
  • CHEN Yunxia ,
  • HE Jie ,
  • XUE Shengran ,
  • ZHANG Xinyi ,
  • ZHENG Jun ,
  • SU Ning
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  • 1(China Academy of Inspection and Quarantine, Beijing 100176, China)
    2(C C TECH (BEIJING) Co.Ltd, Beijing 100176, China)

Received date: 2022-05-18

  Revised date: 2022-06-21

  Online published: 2023-04-28

摘要

寻找天然有效成分以延缓皮肤衰老是近年来人们关注与研究的热点。为研究灵芝孢子粉提取物(Ganoderma lucidum spore extract,GLSE)对新生儿人真皮成纤维细胞(human dermal fibroblasts neonatal,HDFn)氧化损伤保护作用及其抗衰老作用,构建叔丁基过氧化氢(tert-butyl hydroperoxide, TBHP)诱导HDFn氧化损伤衰老模型,测定GLSE对衰老模型的保护作用以及细胞中超氧化物歧化酶(superoxide dismutase, SOD)活性、谷胱甘肽过氧化物酶(glutathione peroxidase, GSH-Px)活性以及丙二醛(malondialdehyde, MDA)水平、线粒体膜电位变化;同时测定衰老相关β-半乳糖苷酶活性以及抗氧化应激相关Nrf2/HO-1通路表达情况。结果显示,GLSE预处理后对TBHP诱导的衰老模型具有保护作用;GLSE作用HDFn后,能够降低MDA含量,提高细胞SOD和GSH-Px活性,稳定细胞线粒体膜电位,并且可以抑制细胞β-半乳糖苷酶活性,激活通路Nrf2/HO-1 mRNA表达。因此,GLSE作用于HDFn后,可以有效地减弱TBHP诱导的氧化损伤,从而达到延缓皮肤衰老的作用。

本文引用格式

刘春媛 , 刘振华 , 陈云霞 , 何婕 , 薛圣然 , 张心怡 , 郑君 , 苏宁 . 灵芝孢子粉提取物延缓皮肤衰老作用研究[J]. 食品与发酵工业, 2023 , 49(7) : 59 -65 . DOI: 10.13995/j.cnki.11-1802/ts.032298

Abstract

Searching for natural active ingredients to delay skin aging is a hot spot in recent years. To study the protective effect and anti-aging effect of Ganoderma lucidum spore extract (GLSE) on HDFn from oxidative damage, the model which tert-butyl hydroperoxide (TBHP) induced oxidative damage and aging of HDFn was constructed. CCK8 method was used to determine the cell survival rate after TBHP induction to determine the protective effect of GLSE on aging model. The activities of superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px), malondialdehyde (MDA) level were measured. Flow cytometry was used to detect the changes of mitochondrial membrane potential after GLSE pretreatment on TBHP-induced oxidative damage. Moreover, the activity of senescence-related β-galactosidase and the expression of Nrf2/HO-1 pathway related to anti-oxidative stress were measured. The results showed that GLSE pretreatment had a protective effect on TBHP induced aging model. After acting on HDFn, GLSE decreased the content of MDA, increased the activities of SOD and GSH-Px. Further studies showed that GLSE significantly stabilized the mitochondrial membrane potential of HDFn, indicating that GLSE could inhibit the mitochondrial damage induced by TBHP. In addition, GLSE suppressed cells β-galactosidase activity, activated antioxidant pathway Nrf2/HO-1 mRNA expression. In conclusion, after GLSE acts on HDFn, it can effectively attenuate the oxidative damage induced by TBHP, thereby delaying skin aging.

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