The Potential of Bioactive Fish Collagen Oligopeptides against Hydrogen Peroxide-Induced NIH/3T3 and HUVEC Damage: The Involvement of the Mitochondria

被引:1
作者
Zhu, Na [1 ,2 ]
Liu, Rui [1 ,3 ]
Xu, Meihong [1 ,4 ]
Li, Yong [1 ,4 ]
机构
[1] Peking Univ, Sch Publ Hlth, Dept Nutr & Food Hyg, Beijing 100191, Peoples R China
[2] Inner Mongolia Med Univ, Coll Publ Hlth, Dept Nutr & Food Hyg, Hohhot 010059, Peoples R China
[3] Peking Univ, Inst Adv Clin Med, Beijing 100191, Peoples R China
[4] Peking Univ, Beijing Key Lab Toxicol Res & Risk Assessment Food, Beijing 100191, Peoples R China
关键词
fish collagen oligopeptides; hydrogen peroxide; inflammation; mitochondria; SALMON ONCORHYNCHUS-KETA; OXIDATIVE STRESS; PEPTIDES; HOMEOSTASIS; METABOLISM; BIOLOGY; SKIN;
D O I
10.3390/nu16071004
中图分类号
R15 [营养卫生、食品卫生]; TS201 [基础科学];
学科分类号
100403 ;
摘要
Extensive in vivo investigations have demonstrated the antioxidant properties of fish collagen oligopeptides (FCOPs). One of the main causes of aging and chronic non-communicable diseases is oxidative stress. Therefore, FCOPs have a broad range of applications in illness prevention and delaying aging from the standpoint of the "food is medicine" theory. However, the mechanisms that underpin the antioxidant activity of FCOPs are not completely understood. The specific objective of this essay was to investigate the antioxidant effect of FCOPs and its possible mechanism at the cellular level. Mouse embryonic fibroblasts NIH/3T3 and human vein endothelial cells (HUVECs) were exposed to 200 mu M hydrogen peroxide containing different concentrations of FCOPs for 4 h and were supplemented with different concentrations of FCOPs for 24 h. Normal growth medium without FCOPs was applied for control cells. An array of assays was used to evaluate the implications of FCOPs on cellular oxidative stress status, cellular homeostasis, inflammatory levels, and mitochondrial function. We found that FCOPs exerted a protective effect by inhibiting reactive oxygen species (ROS) production, enhancing superoxide dismutase (SOD) and endothelial nitric oxide synthase (eNOS) activities and cell viability, inhibiting cell cycle arrest in the G1 phase, suppressing interleukin-1 beta (IL-1 beta), IL-6, matrix metalloproteinase-3 (MMP-3) and intercellular adhesion molecule-1(ICAM-1) secretion, downregulating nuclear factor-kappa B (NF-kappa B) activity, protecting mitochondrial membrane potential, and increasing ATP synthesis and NAD+ activities in both cells. FCOPs had a stronger antioxidant impact on NIH/3T3 than on HUVECs, simultaneously increasing glutathione peroxidase (GSH-Px) activity and decreasing malondialdehyde (MDA) content in NIH/3T3. These findings indicate that FCOPs have antioxidant effects on different tissue cells damaged by oxidative stress. FCOPs were therefore found to promote cellular homeostasis, inhibit inflammation, and protect mitochondria. Meanwhile, better health outcomes will be achieved by thoroughly investigating the effective dose and intervention time of FCOPs, as the absorption efficiency of FCOPs varies in different tissue cells.
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页数:15
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