食品科学 ›› 2021, Vol. 42 ›› Issue (9): 107-114.doi: 10.7506/spkx1002-6630-20200228-317

• 营养卫生 • 上一篇    下一篇

桦木酸对T-2毒素诱导小鼠肝损伤的保护作用

杨成林,黄超,刘娟,黄卫梅,袁志航,易金娥,梁曾恩妮,邬静   

  1. (1.湖南农业大学动物医学院,湖南 长沙 410128;2.畜禽保健湖南省工程研究中心,湖南 长沙 410128;3.湖南省农产品加工研究所,湖南 长沙 410125)
  • 出版日期:2021-05-15 发布日期:2021-06-02
  • 基金资助:
    中国博士后科学基金面上项目(2017M620346);湖南省研究生科研创新项目(CX20190509)

Protective Effect of Betulinic Acid on Liver Injury Induced by T-2 Toxin in Mice

YANG Chenglin, HUANG Chao, LIU Juan, HUANG Weimei, YUAN Zhihang, YI Jin’e, LIANG Zeng’enni, WU Jing   

  1. (1. College of Veterinary Medicine, Hunan Agricultural University, Changsha 410128, China; 2. Hunan Engineering Research Center of Livestock and Poultry Health Care, Changsha 410128, China; 3. Hunan Agricultural Products Processing Institute, Changsha 410125, China)
  • Online:2021-05-15 Published:2021-06-02

摘要: 目的:探讨桦木酸(betulinic acid,BA)对T-2毒素致小鼠肝脏损伤的保护作用及其分子机制。方法:选取60 只成年雄性昆明小鼠随机分为6 组,分别为空白对照组、4 mg/kg mb T-2毒素组、0.25 mg/kg mb BA+T-2组、0.5 mg/kg mb BA+T-2组、1 mg/kg mb BA+T-2组和100 mg/kg mb VE+T-2组。连续灌服BA 14 d后,除空白对照组外,其余各组腹腔注射T-2毒素,建立肝损伤模型。检测小鼠血清谷丙转氨酶(alanine aminotransferase,ALT)、谷草转氨酶(aspartate aminotransferase,AST)、碱性磷酸酶(alkaline phosphatase,ALP)活力以及总蛋白(total protein,TP)质量浓度;苏木精-伊红染色观察肝脏组织病理变化;检测肝组织中总抗氧化能力(total antioxidant capacity,T-AOC)、过氧化氢酶(catalase,CAT)、超氧化物歧化酶(superoxide dismutase,SOD)活力以及谷胱甘肽(glutathione,GSH)和丙二醛(malondialdehyde,MDA)含量;TUNEL染色检测肝细胞的凋亡;Western blot法检测肝组织中Bax、Bcl-2、Caspase-3、Janus激酶2(Janus kinase 2,JAK2)、信号传导与转录激活因子3(signal transducer and activator of transcription 3,STAT3)蛋白的表达量变化。结果:BA预处理能够缓解T-2毒素引起的小鼠血清ALT、AST、ALP活力升高和TP质量浓度的降低;能够升高肝组织中T-AOC,CAT、SOD活力和GSH含量,并降低MDA含量;减少凋亡细胞的数量,使Bcl-2表达量升高,Bax、Caspase-3、JAK2、STAT3表达量降低。结论:BA具有抗氧化能力,可通过JAK2/STAT3通路抑制肝细胞凋亡,进而缓解T-2诱导的小鼠肝脏损伤。

关键词: 桦木酸;T-2毒素;肝损伤;氧化应激;细胞凋亡

Abstract: Objective: To explore the protective effect of betulinic acid (BA) on liver injury induced by T-2 toxin in mice and its underlying molecular mechanism. Methods: Totally 60 adult male Kunming mice were randomly divided into six groups: blank control, 4 mg/kg mb T-2 toxin, 0.25 mg/kg mb BA + T-2, 0.5 mg/kg mb BA + T-2, 1 mg/kg mb BA + T-2 and 100 mg/kg mb vitamin E (VE) + T-2. After 14 days of continuous administration of betulinic acid, T-2 toxin was intraperitoneally injected into all groups except the blank control group to induce liver injury. The activities of alanine aminotransferase (ALT), aspartate aminotransferase (AST) and alkaline phosphatase (ALP) and total protein (TP) concentration in serum were measured. Histopathological changes in the liver were observed by hematoxylin-eosin staining. Total antioxidant capacity (T-AOC), the activities of catalase (CAT) and superoxide dismutase (SOD), and the contents of glutathione (GSH) and malondialdehyde (MDA) in liver tissues were determined. Apoptosis of hepatocytes was detected by TUNEL staining. The protein expression of Bax, Bcl-2, caspase-3, Janus kinase 2 (JAK2) and signal transducer and activator of transcription 3 (STAT3) in liver tissues was evaluated by Western blot. Results: BA pretreatment attenuated the increase in the activities of ALT, AST and ALP and the decrease in TP concentration in serum caused by T-2 toxin. Also, it increased T-AOC, CAT and SOD activity and GSH content, decreased MDA content and the number of apoptotic cells, up-regulated the expression of Bcl-2 protein, and down-regulated the expression of Bax, caspase-3, JAK2, and STAT3 proteins. Conclusion: BA inhibits hepatocyte apoptosis through the JAK2/STAT3 pathway due to its antioxidant capacity, thereby alleviating T-2-induced liver injury in mice.

Key words: betulinic acid; T-2 toxin; liver damage; oxidative stress; apoptosis

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