食品科学

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榛蘑多糖对乙醇所致大鼠血管内皮损伤的保护作用

张俊慧1,陈然然1,丛贺2,沈明花1   

  1. 1. 延边大学医学院
    2. 延边大学
  • 收稿日期:2023-08-18 修回日期:2023-10-07 出版日期:2023-10-20 发布日期:2023-10-20
  • 通讯作者: 沈明花
  • 基金资助:
    国家自然科学基金地区科学基金项目;吉林省中医药管理局中医药科技项目

Protective effects of Armillaria mellea polysaccharides on vascular endothelial cells injury by ethanol in rats

1, 1, 1,   

  • Received:2023-08-18 Revised:2023-10-07 Online:2023-10-20 Published:2023-10-20

摘要: 目的:研究榛蘑多糖(Armillaria mellea polysaccharides)对乙醇所致大鼠血管内膜损伤的保护作用。方法:将40只SD大鼠随机分成4组,分别为正常对照组、损伤组、榛蘑多糖低、高剂量组。除正常对照组外的其余各组均按10 mL/kg体质量灌胃40%的乙醇诱导血管内膜的损伤。榛蘑多糖低、高剂量组分别以100 mg/kg、400 mg/kg体质量灌胃榛蘑多糖,其余组以等体积生理盐水代替,共4 W。苏木精-伊红(hematoxylin-eosin,HE)染色观察颈动脉组织病理变化;检测血清甘油三酯(triglyceride, TG)、总胆固醇(total cholesterol, T-CHO)、低密度脂蛋白胆固醇(low density lipoprotein cholesterol, LDL-C)、高密度脂蛋白胆固醇(high density lipoprotein cholesterol, HDL-C)、内皮型一氧化氮合酶(endothelial nitric oxide synthase, eNOS)、诱导型一氧化氮合酶(inducible nitric oxide synthase, iNOS)、一氧化氮(nitric oxide, NO)、内皮素-1(endothelin 1, ET-1)、超氧化物歧化酶(superoxide dismutase, SOD)和丙二醛(malondialdehyde, MDA)水平。此外,以600 mmol/mL的乙醇诱导人脐静脉内皮细胞损伤模型,观察不同剂量(100 μg/mL、400 μg/mL)的榛蘑多糖对细胞活性氧(reactive oxygen species, ROS)、线粒体跨膜电位、细胞凋亡以及凋亡相关蛋白B淋巴细胞瘤2 (B cell lymphoma 2, Bcl2)、Bcl2相关x蛋白(Bcl 2 associated x protein, Bax)和半胱天冬氨酸蛋白酶3(cysteinyl aspartate specific proteinase 3,caspase3)表达的影响。结果:榛蘑多糖减轻乙醇所致的血管内膜损伤,降低T-CHO、TG、LDL-C、iNOS、NO、ET-1和MDA水平,提高HDL-C和SOD活性。在体外,榛蘑多糖降低细胞活性氧水平,抑制乙醇所致的线粒体跨膜电位的下降和细胞凋亡,并提高Bcl2/Bax,下调Cleaved caspase3表达水平。结论:榛蘑多糖对乙醇诱导的大鼠血管内膜损伤有保护作用,其机制可能与其降脂、抗氧化和抗凋亡作用有关。

关键词: 榛蘑多糖, 血管内皮, 乙醇

Abstract: Objective: To study the protective effect of hazel mushroom polysaccharides (Armillaria mellea polysaccharides) against ethanol-induced endothelial injury in rats. Methods: Forty SD rats were randomly divided into four groups, which were the normal control group, the injury group, and Armillaria mellea polysaccharides low and high dose groups. All groups except the normal control group were gavaged with 40% ethanol at 10 mL/kg body mass to induce endothelial injury. The low and high dose groups were gavaged with 100 mg/kg and 400 mg/kg body mass of Armillaria mellea polysaccharides, respectively, and the rest of the groups were substituted with an equal volume of saline for a total of 4 W. The histopathological changes of carotid arteries were observed by hematoxylin-eosin (HE) staining; Triglycerides (TG), total cholesterol (T-CHO), low-density lipoprotein cholesterol (LDL-C), high-density lipoprotein cholesterol (HDL-C), endothelial nitric oxide synthase (eNOS), inducible nitric oxide synthase (iNOS), nitric oxide (NO), endothelin 1 (ET-1), superoxide dismutase (SOD),and malondialdehyde (MDA) levels were detected. In addition, human umbilical vein endothelial cell injury was induced by 600 mmol/mL ethanol, and the effects of different doses (100 g/mL, 400 g/mL) of Armillaria mellea polysaccharides on the levels of reactive oxygen species (ROS), mitochondrial transmembrane potential, apoptosis, apoptosis-associated proteins (B cell lymphoma 2, Bcl2) , Bcl 2 associated x protein (Bax), and cysteinyl aspartate specific proteinase 3 (caspase3) were investigated. Results: Armillaria mellea polysaccharides attenuated ethanol-induced endothelial injury, decreased T-CHO, TG, LDL-C, iNOS, NO, ET-1, and MDA levels, and increased HDL-C and SOD activities. In vitro, Armillaria mellea polysaccharides reduced cellular reactive oxygen species levels, inhibited ethanol-induced decreases in mitochondrial transmembrane potential and apoptosis, and increased Bcl2/Bax and down-regulated Cleaved Caspase3 expression levels. Conclusion: Armillaria mellea polysaccharides have a protective effect on ethanol-induced endothelial injury in rats, and the mechanism may be related to their lipid-lowering, antioxidant, and anti-apoptotic effects.

Key words: Armillaria mellea polysaccharides, vascular endothelium, ethanol

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