食品科学 ›› 2020, Vol. 41 ›› Issue (19): 198-203.doi: 10.7506/spkx1002-6630-20190816-179

• 营养卫生 • 上一篇    下一篇

桑叶生物碱对D-半乳糖诱导氧化损伤模型小鼠肾脏的改善作用

杨忠敏,沈以红,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:2020-10-15 发布日期:2020-10-23
  • 基金资助:
    现代农业产业技术体系建设专项(CARS-18)

Mulberry Leaf Alkaloids Improve D-Galactose-Induced Oxidative Damage in the Mouse Kidney

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

  1. (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:2020-10-15 Published:2020-10-23

摘要: 目的:探讨桑叶生物碱对肾脏氧化损伤是否具有改善作用,旨在为桑叶生物碱的开发利用提供理论依据。方法:采用D-半乳糖诱导建立小鼠氧化损伤模型,然后灌胃不同剂量的桑叶生物碱,于第4周末测定小鼠肾脏组织中蛋白羰基(protein carbonyl,PCO)、晚期蛋白氧化产物(advanced oxidation protein products,AOPP)、8-异前列腺素F2α(8-iso-prostaglandin F2α,8-iso-PGF2α)、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)的水平及超氧化物歧化酶(superoxide dismutase,SOD)、谷胱甘肽过氧化物酶(glutathione peroxidase,GSH-Px)、还原型烟酰胺腺嘌呤二核苷酸磷酸(reduced nicotinamide adenine dinucleotide phosphate,NADPH)氧化酶(NADPH oxidase,NOX)、蛋白激酶C(protein kinase C,PKC)的酶活力。结果:与模型对照组相比,桑叶生物碱高剂量组(200 mg/kg mb)能使小鼠肾脏组织中蛋白氧化产物PCO、AOPP分别降低37.27%、42.71%(P<0.01);脂质氧化产物8-iso-PGF2α降低51.07%(P<0.01);DNA氧化产物8-OH-dG、5-OH-dC分别降低31.66%、18.91%(P<0.01);同时,桑叶生物碱高剂量组也使肾脏组织中抗氧化酶SOD、GSH-Px活力分别升高83.74%、59.31%(P<0.01);NOX、PKC活力分别降低41.21%、40.65%(P<0.01)。结论:桑叶生物碱对D-半乳糖诱导的小鼠肾脏氧化损伤具有较好改善作用,其机制可能与升高SOD、GSH-Px活力和抑制NOX、PKC活力,进而减少机体活性氧自由基过量产生有关。

关键词: 桑叶生物碱;D-半乳糖;氧化应激;肾损伤;机制

Abstract: Objective: To explore whether mulberry leaf alkaloids can improve oxidative damage in the kidney of mice for the purpose of providing a theoretical basis for the development and utilization of mulberry leaf alkaloids. Methods: A mouse model of renal oxidative damage was induced by D-galactose (D-Gal) and the model mice were administered with different doses of mulberry leaf alkaloids for 4 consecutive weeks. At the end of the 4th week, the levels of protein carbonyl (PCO), advanced oxidation protein products (AOPP), 8-iso-prostaglandin F2α (8-iso-PGF2α), 8-hydroxy-2’-desoxyguanosine (8-OH-dG) and 5-hydroxy-2’-deoxycotosine (5-OH-dC), and the activity of total superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), reduced nicotinamide adenine dinucleotide phosphate oxidase (NOX), and protein kinase C (PKC) in the kidney was measured. Results: Compared with the model control group, high-dose mulberry leaf alkaloids (200 mg/kg mb) could reduce the protein oxidation products PCO and AOPP in the kidney tissues of mice by 37.27% and 42.71%, respectively (P < 0.01), the lipid oxidation product 8-iso-PGF2α by 51.07% (P < 0.01), and the DNA oxidation products 8-OH-dG and 5-OH-dC by 31.66% and 18.91%, respectively (P < 0.01); increase the activity of antioxidant enzymes SOD and GSH-Px by 83.74% and 59.31%, respectively; and decrease NOX and PKC activity by 41.21% and 40.65%, respectively (P < 0.01). Conclusion: Mulberry leaf alkaloids have a good effect on improving D-Gal-induced oxidative damage in the mouse kidney, and the underlying mechanism may be related to increasing the activity of SOD and GSH-Px and inhibiting the activity of NOX and PKC, thereby reducing the overproduction of reactive oxygen species (ROS) in the body.

Key words: mulberry leaf alkaloids; D-galactose; oxidative damage; kidney damage; mechanism

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