畜牧兽医学报 ›› 2022, Vol. 53 ›› Issue (2): 637-645.doi: 10.11843/j.issn.0366-6964.2022.02.030

• 临床兽医 • 上一篇    下一篇

番茄红素对壬基酚诱导小鼠脾损伤的保护作用及机制研究

杨少青1,2,3, 邵春艳1,2,3, 周彬1,2,3, 宋泉江1,2,3, 王晓杜1,2,3*, 宋厚辉1,2,3*, 姜胜1,2,3*   

  1. 1. 浙江农林大学动物科技学院、动物医学院, 杭州 311300;
    2. 浙江省畜禽绿色生态健康养殖应用 技术研究重点实验室, 杭州 311300;
    3. 动物健康互联网检查技术浙江省工程实验室, 杭州 311300
  • 收稿日期:2021-03-24 出版日期:2022-02-23 发布日期:2022-03-02
  • 通讯作者: 姜胜,主要从事动物麻醉与镇痛研究,E-mail:cjsheng@zafu.edu.cn;王晓杜,主要从事动物病毒学研究,E-mail:xdwang@zafu.edu.cn;宋厚辉,主要从事动物疫病诊断研究,E-mail:songhh@zafu.edu.cn
  • 作者简介:杨少青(1996-),女,浙江温州人,硕士生,主要从事畜禽毒理与内科疾病研究,E-mail:1051672039@qq.com
  • 基金资助:
    国家自然科学基金(31602119);浙江省重点实验室开放项目(S2019018);浙江农林大学科研启动项目(2015FR042)

Protective Effect and Mechanism of Lycopene on Spleen Injury Induced by Nonylphenol in Mice

YANG Shaoqing1,2,3, SHAO Chunyan1,2,3, ZHOU Bin1,2,3, SONG Quanjiang1,2,3, WANG Xiaodu1,2,3*, SONG Houhui1,2,3*, JIANG Sheng1,2,3*   

  1. 1. College of Animal Science and Technology·College of Veterinary Medicine, Zhejiang A&F University, Hangzhou 311300, China;
    2. Key Laboratory of Applied Technology on Green-Eco-Healthy Animal Husbandry of Zhejiang Province, Hangzhou 311300, China;
    3. Zhejiang Provincial Engineering Laboratory for Animal Health Inspection and Internet Technology, Hangzhou 311300, China
  • Received:2021-03-24 Online:2022-02-23 Published:2022-03-02

摘要: 探讨番茄红素(lycopene,LYC)对壬基酚(nonylphenol,NP)亚慢性中毒诱导小鼠脾损伤的保护作用及机制。将40只清洁级ICR小鼠随机分为对照组(CON)、中毒组(NPG)、番茄红素对照组(LCG)和番茄红素干预组(LNG)。对照组,每天8:30灌服玉米油0.1 mL,2 h后重复操作;中毒组,每天8:30灌服玉米油0.1 mL,2 h后灌服150 mg·kg-1壬基酚溶液;番茄红素对照组,每天8:30灌服5 mg·kg-1番茄红素,2 h后灌服0.1 mL玉米油;番茄红素干预组,每天8:30灌服5 mg·kg-1番茄红素,2 h后灌服150 mg·kg-1壬基酚溶液。各组连续进行相应灌胃处理30 d后,记录小鼠体重,颌下静脉采集血样,并对小鼠进行安乐死,剖解后采集小鼠脾称重,分析小鼠日均增重以及脾体系数的组间差异;检查血清中免疫细胞因子IL-2、IFN-γ和TNF-α的变化;检测脾氧化与抗氧化指标MDA、T-AOC、CAT、GSH-Px和SOD的差异变化;检测凋亡通路p53/Bcl-2各蛋白表达的差异。结果表明,与NPG相比,经过LYC干预后NP暴露小鼠日均增重显著升高(P<0.05),血清免疫细胞因子含量和脾抗氧化酶活性显著升高(P<0.05);LYC干预后小鼠脾凋亡通路关键分子Akt、p-Akt和Bcl-2蛋白表达水平显著升高(P<0.05),p53和Bax蛋白表达水平显著降低(P<0.05)。结果提示,LYC对NP诱导的小鼠脾损伤具有保护作用,这与LYC增强脾抗氧化能力,抑制脾细胞凋亡有关。

关键词: 番茄红素, 壬基酚, 氧化应激, 凋亡

Abstract: The study aimed to investigate the protective effect and mechanism of lycopene (LYC) on subchronic poisoning of nonylphenol (NP) in spleen of mice. Forty ICR mice were randomly divided into four groups including control group (CON), poisoning group (NPG), lycopene control group (LCG) and lycopene intervention group (LNG). Mice in CON were given 0.1 mL corn oil at 8:30 every day, and the operation was repeated after two hours; mice in NPG were administrated 0.1 mL corn oil at 8:30 every day, and then were given 150 mg·kg-1 NP two hours later; mice in LCG were given 5 mg·kg-1 LYC at 8:30 every day, and then were given 0.1 mL corn oil two hours later; mice in LNG were given 5 mg·kg-1 LYC at 8:30 every day, and then were administrated 150 mg·kg-1 NP two hours later. After 30 days of consecutive gavage, the weight of mice was recorded, blood samples were collected from submaxillary vein, then mice were euthanized, and the spleen of mice was collected and weighed after dissection, and the difference between the groups of weight growth rate and spleen body coefficient were analyzed. The changes of immunity cytokines IL-2, IFN-γ and TNF-α in serum were examined, and the spleen oxidation and anti oxidative indexes MDA, T-AOC, CAT, GSH-Px and SOD was observed, and the protein expression in p53/Bcl-2 apoptosis pathway was detected. The results showed that compared with NPG, the weight growth rate of mice was significantly increased after LYC treatment (P<0.05), serum cytokines and spleen antioxidant enzyme activity were significantly increased (P<0.05); the expression levels of key molecules of apoptosis pathway Akt, p-Akt and Bcl-2 protein in spleen of mice after LYC treatment were significantly increased (P<0.05), and the expression level of p53 and Bax protein was significantly decreased (P<0.05). LYC has protective effect on NP induced spleen injury in mice, which was related to enhancing the anti-oxidation ability of spleen and inhibiting apoptosis of spleen cells.

Key words: lycopene, nonylphenol, oxidative stress, apoptosis

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