食品科学 ›› 2019, Vol. 40 ›› Issue (7): 156-162.doi: 10.7506/spkx1002-6630-20180326-340

• 营养卫生 • 上一篇    下一篇

纳豆激酶对大鼠酒精性肝损伤的改善效果及免疫调节作用

卓怡云,吕 婧,刘 颖,王子龙,刘 曼,梁 惠   

  1. 1.青岛大学公共卫生学院,山东 青岛 266021;2.青岛大学基础医学院,山东 青岛 266071
  • 出版日期:2019-04-15 发布日期:2019-05-05
  • 基金资助:
    国家自然科学基金面上项目(81573137);山东省重点研发计划项目(2017GSF18167);汤臣倍健营养科学研究基金项目(2016-102)

Nattokinase Alleviates Alcoholic Liver Injury and Modulates Immune Function in Rats

ZHUO Yiyun, Lü Jing, LIU Ying, WANG Zilong, LIU Man, LIANG Hui   

  1. 1. School of Public Health, Qingdao University, Qingdao 266021, China; 2. School of Basic Medicine, Qingdao University, Qingdao 266071, China
  • Online:2019-04-15 Published:2019-05-05

摘要: 目的:探讨纳豆激酶对大鼠酒精性肝损伤的改善效果及免疫调节作用。方法:雄性Wistar大鼠随机分为5 组,正常对照组(生理盐水灌胃)、酒精模型组(酒精体积分数56%的白酒灌胃:第1周灌胃6 mL/(kg?d mb),第2周灌胃8 mL/(kg?d mb),第3周灌胃10 mL/(kg?d mb),第4~10周灌胃11 mL/(kg?d mb))、纳豆激酶对照组(灌胃530.39 FU/(kg?d mb)纳豆激酶)、纳豆激酶干预组(灌胃530.39 FU/(kg?d mb)纳豆激酶+酒精)、甘利欣干预组(灌胃200 mg/(kg?d mb)甘利欣+酒精);后两组酒精剂量同酒精模型组,实验持续10 周。苏木精-伊红染色观察肝脏组织形态结构,透射电子显微镜观察肝细胞超微结构;测定血清谷丙转氨酶(alanine aminotransferase,ALT)、谷草转氨酶(aspartate aminotransferase,AST)、γ-谷氨酰转肽酶(gamma-glutamyl transpeptidase,GGT)、胆碱酯酶(cholinesterase,CHE)活力;计算脾指数,流式细胞术检测大鼠外周血中CD4+、CD8+ T淋巴细胞亚群和自然杀伤(natural killer,NK)细胞比例。结果:酒精模型组大鼠肝组织形态结构和肝细胞超微结构均出现明显的病变损伤,纳豆激酶和甘利欣干预后得到显著改善。与酒精模型组相比,纳豆激酶干预组和甘利欣干预组大鼠血清ALT、AST、GGT活力显著下降(P<0.05),CHE活力有一定上升趋势。与酒精模型组相比,纳豆激酶干预组和甘利欣干预组大鼠脾指数、CD3+CD4+ T淋巴细胞比例、CD3+CD8+ T淋巴细胞比例均显著升高(P<0.05),TCRαβ+CD161a+ NK细胞比例有不同程度的上升趋势。结论:纳豆激酶对大鼠酒精性肝损伤有一定改善效果,其机制可能与调节CD4+、CD8+ T淋巴细胞、NK细胞等免疫细胞比例,提高机体免疫调节作用有关。

关键词: 纳豆激酶, 酒精性肝损伤, 免疫调节, CD4+、CD8+ T淋巴细胞, 自然杀伤细胞

Abstract: Objective: In order to investigate the effect of nattokinase on the alleviation of alcoholic liver injury and its immunomodulatory effect in rats. Methods: Male Wistar rats were randomly divided into five groups: normal control (intragastrically administered with normal saline), model (gavaged with Erguotou liquor (56% alcohol, V/V) at 6 mL/(kg·d mb) for the first week, at 8 mL/(kg·d mb) for the second week, at 10 mL/(kg·d mb) for the third week, and at 11 mL/(kg·d mb) for the fourth to the tenth week), nattokinase control (orally administered with 530.39 FU/(kg·d mb) nattokinase), nattokinase intervention (administered with 530.39 FU/(kg·d mb) nattokinase and alcohol), and diammonium glycyrrhizinate intervention (administered with 200 mg/(kg·d mb) diammonium glycyrrhizinate and alcohol). The same dose of alcohol was given to the latter two groups as that for the model group. The experiment lasted for 10 weeks. Morphological examination of liver tissue was performed by hematoxylin and eosin (H&E) staining, and the ultrastructure of liver cells was observed by transmission electron microscopy. Serum alanine aminotransferase (ALT), aspartate aminotransferase (AST), glutamyl transpeptidase (GGT), and cholinesterase (CHE) activities were determined. The spleen index was calculated and the number of CD4+ and CD8+ T lymphocyte subsets and natural killer (NK) cells in the peripheral blood of rats was determined by flow cytometry. Results: The morphological structure of liver tissue and the ultrastructure of liver cells in the model group showed obvious pathological changes and damage, which were improved significantly after nattokinase and diammonium glycyrrihizinate intervention. Compared with the model group, the levels of serum ALT, AST and GGT decreased significantly (P < 0.05) whereas CHE increased in the nattokinase intervention and diammonium glycyrrhizinate intervention groups. Moreover, the spleen index and the percentage of CD3+CD4+ T cells and CD3+CD8+ T cells increased significantly (P < 0.05), and the percentage of TCRαβ+CD161a+ NK cell also rose in different degrees in the nattokinase intervention and diammonium glycyrrhizinate intervention groups. Conclusion: Nattokinase attenuates alcoholic liver injury in rats, likely by regulating the proportion of immune effector cells such as CD4+, CD8+ T and NK cells and enhancing immune function.

Key words: nattokinase, alcoholic liver injury, immunomodulation, CD4+ and CD8+ T lymphocytes, natural killer cells

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