食品科学 ›› 2020, Vol. 41 ›› Issue (5): 135-142.doi: 10.7506/spkx1002-6630-20190226-195

• 营养卫生 • 上一篇    下一篇

桑叶生物碱对D-半乳糖诱导小鼠生物大分子氧化损伤的改善作用及机理

杨忠敏,王祖文,黄先智,丁晓雯   

  1. (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:2020-03-15 发布日期:2020-03-23
  • 基金资助:
    公益性行业(农业)科研专项(201403049);现代农业产业技术体系建设专项(CARS-18)

Effect and Underlying Mechanism of Mulberry Leaf Alkaloid on Improving D-Galactose-Induced Oxidative Damage in Mice

YANG Zhongmin, WANG Zuwen, HUANG Xianzhi, DING Xiaowen   

  1. (1. Chongqing Key Laboratory of Agricultural Products Processing and Store, 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:2020-03-15 Published:2020-03-23

摘要: 目的:研究桑叶生物碱对D-半乳糖(D-galactose,D-Gal)诱导小鼠生物大分子氧化损伤的改善作用,并从机体自身抗氧化防御系统角度初步探讨其作用机理。方法:以D-Gal诱导建立氧化应激模型,实验保留10 只小鼠作为正常对照组,并将建模成功的小鼠随机分为模型对照组、阳性药物组(还原型谷胱甘肽,200 mg/kg mb)以及桑叶生物碱低、中、高剂量组(50、100、200 mg/kg mb)。连续灌胃4 周,测定小鼠体质量、摄食量;血浆中生物大分子氧化损伤标志物含量及抗氧化相关指标,包括8-异前列腺素F2α(8-iso-prostaglandin F2α,8-iso-PGF2α)、蛋白羰基(protein carbonyl,PCO)、晚期蛋白氧化产物(advanced oxidation protein products,AOPP)、3-硝基络氨酸(3-nitrotyrosine,3-NT)、8-羟基鸟嘌呤(8-hydroxy-2’-desoxyguanosine,8-OH-dG)、5-羟基胞嘧啶(5-hydroxy-2’-deoxycotosine,5-OH-dC)、总超氧化物歧化酶(total superoxide dismutase,T-SOD)、谷胱甘肽过氧化物酶(glutathione peroxidase,GSH-Px)、金属硫蛋白(metallothionein,MT)、硫氧还蛋白(thioredoxin,Trx)水平及总抗氧化能力(total antioxidant capability,TAC)。结果:与模型组对比,桑叶生物碱高剂量组小鼠体质量、摄食量、摄食率明显增加;桑叶生物碱中、高剂量组血浆中8-iso-PGF2α、PCO、AOPP、3-NT、8-OH-dG、5-OH-dC含量均显著降低(P<0.05),T-SOD、GSH-Px的活力、MT、Trx的含量、TAC均显著增加(P<0.05),并呈一定的量效关系。其中高剂量组8-iso-PGF2α、PCO、AOPP、3-NT、8-OH-dG、5-OH-dC含量分别极显著降低了83.46%、35.43%、61.70%、63.65%、65.02%、57.90%(P<0.05);T-SOD、GSH-Px活力、MT、Trx含量、TAC分别极显著增加至模型对照组的1.47、2.96、1.74、1.37、1.63 倍(P<0.05),均达到了正常对照组水平(P>0.05)。结论:桑叶生物碱能有效改善小鼠脂质、DNA、蛋白质氧化损伤;其作用机理可能与调节机体抗氧化酶活力和非酶抗氧化剂含量,增强机体抗氧化防御系统能力有关。

关键词: 桑叶生物碱, D-半乳糖, 生物大分子, 氧化损伤

Abstract: Objective: To investigate the improving effect of mulberry leaf alkaloid (MLA) on D-galactose (D-Gal)-induced oxidative damage in mice, and to illustrate its underlying mechanism from the perspective of the animal’s own antioxidant defense system. Methods: An oxidative stress model was induced by D-Gal. Ten normal mice were served as the normal control. The model mice were randomly divided into model control, positive control (glutathione at 200 mg/kg mb) and low-, medium- and high-dose MLA treatment groups (50, 100, and 200 mg/kg mb). After intragastric administration for 4 consecutive weeks, body mass, food intake and food utilization of the mice were measured. The levels of 8-iso-prostaglandin F2α (8-iso-PGF2α), protein carbonyl (PCO), advanced oxidation protein products (AOPP), 3-nitrotyrosine (3-NT), 8-hydroxy-2’-desoxyguanosine (8-OH-dG), 5-hydroxy-2’-deoxycotosine (5-OH-dC) in plasma were measured by enzyme-linked immunosorbent assay test kit. The activities of total superoxide dismutase (T-SOD) and glutathione peroxidase (GSH-Px), and the levels of metallothionein (MT) and thioredoxin (Trx), as well as total antioxidant capacity (TAC) in plasma were measured by using commercial test kits. Results: Compared with the model control group, body mass, food intake and food utilization of mice in the high-dose MLA group were significantly increased. The plasma contents of 8-iso-PGF2α, PCO, AOPP, 3-NT, 8-OH-dG, and 5-OH-dC in the medium- and high-dose MAL groups were significantly decreased (P < 0.05), and the activities of T-SOD and GSH-Px, the contents of MT and Trx, and TAC value were significantly increased (P < 0.05); all these effects were dose-dependent. In the high-dose group, the contents of 8-iso-PGF2α, PCO, AOPP, 3-NT, 8-OH-dG, and 5-OH-dC were significantly reduced by 83.46%, 35.43%, 61.70%, 63.65%, 65.02%, and 57.90%, respectively (P < 0.05). In addition, T-SOD, GSH-Px, MT, Trx, and TAC increased by 1.47, 2.96, 1.74, 1.37 and 1.63 times, respectively (P < 0.05), all of which reached the normal levels (P > 0.05). Conclusion: Mulberry leaf alkaloid can effectively improve lipid, DNA and protein oxidative damage in mice. The underlying mechanism may be related to regulating antioxidant enzyme activities and non-enzyme antioxidant contents, and enhancing the antioxidant defense system.

Key words: mulberry leaf alkaloid, D-galactose, biomacromolecule, oxidative damage

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