桑叶生物碱粗提物对D-半乳糖诱导的小鼠蛋白氧化损伤的改善作用

doi:10.7506/spkx1002-6630-20190731-430

食品科学 ›› 2020, Vol. 41 ›› Issue (17): 182-187.doi: 10.7506/spkx1002-6630-20190731-430

桑叶生物碱粗提物对D-半乳糖诱导的小鼠蛋白氧化损伤的改善作用

杨忠敏，沈以红，黄先智，王祖文，丁晓雯

（1.西南大学食品科学学院，重庆市农产品加工重点实验室，食品科学与工程国家级实验教学示范中心，重庆 400716；2.西南大学科技处，重庆 400716）

出版日期:2020-09-15 发布日期:2020-09-16
基金资助:
现代农业产业技术体系建设专项（CARS-18）

Effect of Crude Alkaloids from Mulberry Leaves on Improving D-Galactose-Induced Oxidative Protein Damage in Mice

YANG Zhongmin, SHEN Yihong, HUANG Xianzhi, WANG Zuwen, DING Xiaowen

(1. Chongqing Key Laboratory of Agricultural Products Processing, National Demonstration Center for Experimental Food Science and Technology Education, College of Food Science, Southwest University, Chongqing 400716, China; 2. Science and Technology Department, Southwest University, Chongqing 400716, China)

Online:2020-09-15 Published:2020-09-16

摘要/Abstract

摘要： 目的：探讨桑叶生物碱改善小鼠蛋白氧化损伤作用效果与机理，旨在为桑叶生物碱的开发利用提供理论依据。方法：采用D-半乳糖（D-galactose，D-Gal）诱导建立小鼠氧化损伤模型，灌胃不同剂量的桑叶生物碱，于第8周末测定小鼠血浆蛋白羰基（protein carbonyl，PCO）、晚期蛋白氧化产物（advanced oxidation protein products，AOPP）、3-硝基酪氨酸（3-nitrotyrosine，3-NT）含量及超氧化物歧化酶（superoxide dismutase，SOD）、谷胱甘肽过氧化物酶（glutathione peroxidase，GSH-Px）、醌氧化还原酶1（NAD(P)H quinine oxidoreductase 1，NQO1）活力，实时荧光定量聚合酶链式反应测定肝脏组织SOD、GSH-Px、NQO1、核因子E2相关因子2（nuclear erythroid related factor 2，Nrf2）、Kelch样环氧氯丙烷相关蛋白1（Kelch like ECH-associated protein-1，Keap1）mRNA表达情况。结果：与模型对照组相比，桑叶生物碱高剂量组（200 mg/kg mb）小鼠血浆中PCO、AOPP、3-NT水平分别降低36.43%、61.81%、58.13%（P＜0.01）；血浆中的SOD、GSH-Px、NQO1活力分别提高48.89%、167.17%、85.12%（P＜0.01）。同时，桑叶生物碱高剂量组肝脏中SOD1、SOD2、GSH-Px、NQO1、Nrf2 mRNA相对表达量分别增加96.96%、94.26%、116.71%、101.51%、63.01%（P＜0.01），Keap1 mRNA相对表达量下降33.54%（P＜0.01）。结论：桑叶生物碱可能通过调控Nrf2/Keap1氧化应激信号通路实现对D-Gal诱导的小鼠蛋白氧化损伤的保护作用。

关键词: 桑叶生物碱；D-半乳糖；蛋白质；氧化损伤；核因子E2相关因子2/Kelch样环氧氯丙烷相关蛋白1信号通路

Abstract: Objective: To explore the effect of alkaloids from mulberry leaves on improving oxidative protein damage in mice and the underlying mechanism for the purpose of providing a theoretical basis for the development and utilization of alkaloids from mulberry leaves. Methods: A mouse model of oxidative damage was induced by D-galactose (D-Gal) and administered with different doses of mulberry leaf alkaloids. At the end of the 8th week, the contents of protein carbonyl (PCO), advanced oxidation protein products (AOPP) and 3-nitrotyrosine (3-NT), and the enzyme activity levels of superoxide dismutase (SOD), glutathione peroxidase (GSH-Px) and NAD(P)H quinine oxidoreductase 1 (NQO1) in plasma were measured. The mRNA expression of SOD, GSH-Px, NQO1, nuclear erythroid related factor 2 (Nrf2) and Kelch-like ECH-associated protein-1 (Keap1) in liver tissues were also detected by real-time polymerase chain reaction (qPCR). Results: Compared with the model control group, the plasma PCO, AOPP and 3-NT levels of mice decreased by 36.43%, 61.81% and 58.13%, respectively after intragastric administration of high-dose mulberry leaf alkaloids (200 mg/kg mb) (P < 0.01). However, the activity of SOD, GSH-Px and NQO1 in plasma increased by 48.89%, 167.17% and 85.12% (P < 0.01). Meanwhile, high-dose mulberry leaf alkaloids also increased the mRNA expression of SOD1, SOD2, GSH-Px, NQO1 and Nrf2 in the liver by 96.96%, 94.26%, 116.71%, 101.51% and 63.01%, respectively (P < 0.01), but decreased the mRNA level of Keap1 by 33.54% (P < 0.01). Conclusion: Mulberry leaf alkaloids have a protective effect on D-Gal-induced oxidative protein damage in mice via adjusting Keap1/Nrf2 signal pathway.

Key words: mulberry leaf alkaloids; D-galactose; protein; oxidative damage; nuclear erythroid related factor 2/Kelch-like ECH-associated protein-1 signaling pathway

中图分类号:

R285.5

杨忠敏，沈以红，黄先智，王祖文，丁晓雯. 桑叶生物碱粗提物对D-半乳糖诱导的小鼠蛋白氧化损伤的改善作用[J]. 食品科学, 2020, 41(17): 182-187.

YANG Zhongmin, SHEN Yihong, HUANG Xianzhi, WANG Zuwen, DING Xiaowen. Effect of Crude Alkaloids from Mulberry Leaves on Improving D-Galactose-Induced Oxidative Protein Damage in Mice[J]. FOOD SCIENCE, 2020, 41(17): 182-187.

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桑叶生物碱粗提物对D-半乳糖诱导的小鼠蛋白氧化损伤的改善作用

Effect of Crude Alkaloids from Mulberry Leaves on Improving D-Galactose-Induced Oxidative Protein Damage in Mice

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