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利用安康鱼皮肤中的胶原蛋白肽通过调节Nrf2途径和NLRP3信号改善高脂饮食喂养小鼠的肾脏损伤。

Using Collagen Peptides From the Skin of Monkfish () to Ameliorate Kidney Damage in High-Fat Diet Fed Mice by Regulating the Nrf2 Pathway and NLRP3 Signaling.

作者信息

Miao Bingtao, Zheng Jiawen, Zheng Guoping, Tian Xiaoxiao, Zhang Wen, Yuan Falei, Yang Zuisu

机构信息

Zhejiang Provincial Engineering Technology Research Center of Marine Biomedical Products, School of Food and Pharmacy, Zhejiang Ocean University, Zhoushan, China.

Zhoushan Institute for Food and Drug Control, Zhoushan, China.

出版信息

Front Nutr. 2022 Feb 10;9:798708. doi: 10.3389/fnut.2022.798708. eCollection 2022.

DOI:10.3389/fnut.2022.798708
PMID:35223948
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8866304/
Abstract

BACKGROUND

Oxidative stress and inflammation play important roles in high-fat diet (HFD) induced kidney damage. Previous studies show that the collagen extracted from the skin of monkfish () with pepsin (pepsin-solubilized collagen, PSC) exhibits good biological activities. This study investigates the protective effect of PSCP against chronic kidney injury in HFD-fed mice.

METHODS

Pepsin-solubilized collagen was further hydrolyzed into collagen peptides, and the compound with the best 2,2-diphenyl-1-picrylhydrazyl (DPPH) clearance rate was named pepsin-solubilized collagen peptide (PSCP). A group of mice were fed an HFD for 4 weeks, and then for another 6 weeks PSCP was added to their diet at the amount of either 100 or 200 mg/kg.

RESULTS

Pepsin-solubilized collagen peptide treatment (200 mg/kg) reduced the mice's serum levels of uric acid (UA), creatinine (CRE), and blood urea nitrogen (BUN) by 27, 20, and 37%, respectively. This treatment also remarkably improved renal histopathology. Moreover, the activities of superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), and catalase (CAT) were increased by 96, 52, and 74%, respectively, and decreased the malondialdehyde (MDA) level by 36%. Additionally, PSCP activated the Nrf2 pathway and inhibited NLRP3 signaling to significantly reduce the levels of inflammatory cytokines IL-1β, IL-6, and TNF-α.

CONCLUSIONS

Our results indicate that compound PSCP has the potential to prevent or control chronic kidney damage.

摘要

背景

氧化应激和炎症在高脂饮食(HFD)诱导的肾损伤中起重要作用。先前的研究表明,用胃蛋白酶从安康鱼皮中提取的胶原蛋白(胃蛋白酶可溶胶原蛋白,PSC)具有良好的生物活性。本研究调查了胃蛋白酶可溶胶原蛋白肽(PSCP)对高脂饮食喂养小鼠慢性肾损伤的保护作用。

方法

将胃蛋白酶可溶胶原蛋白进一步水解成胶原肽,将2,2-二苯基-1-苦基肼(DPPH)清除率最佳的化合物命名为胃蛋白酶可溶胶原蛋白肽(PSCP)。一组小鼠喂食高脂饮食4周,然后在接下来的6周内,以100或200mg/kg的量将PSCP添加到它们的饮食中。

结果

胃蛋白酶可溶胶原蛋白肽处理(200mg/kg)使小鼠血清尿酸(UA)、肌酐(CRE)和血尿素氮(BUN)水平分别降低了27%、20%和37%。这种处理还显著改善了肾脏组织病理学。此外,超氧化物歧化酶(SOD)、谷胱甘肽过氧化物酶(GSH-Px)和过氧化氢酶(CAT)的活性分别提高了96%、52%和74%,丙二醛(MDA)水平降低了36%。此外,PSCP激活了Nrf2通路并抑制了NLRP3信号传导,以显著降低炎性细胞因子IL-1β、IL-6和TNF-α的水平。

结论

我们的结果表明,化合物PSCP有预防或控制慢性肾损伤的潜力。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8b92/8866304/81f9753e68f7/fnut-09-798708-g0005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8b92/8866304/09c6c020d77e/fnut-09-798708-g0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8b92/8866304/ff786c16fdce/fnut-09-798708-g0002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8b92/8866304/3743117f9620/fnut-09-798708-g0003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8b92/8866304/f8ff26be658d/fnut-09-798708-g0004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8b92/8866304/81f9753e68f7/fnut-09-798708-g0005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8b92/8866304/09c6c020d77e/fnut-09-798708-g0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8b92/8866304/ff786c16fdce/fnut-09-798708-g0002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8b92/8866304/3743117f9620/fnut-09-798708-g0003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8b92/8866304/f8ff26be658d/fnut-09-798708-g0004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8b92/8866304/81f9753e68f7/fnut-09-798708-g0005.jpg

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