食品科学 ›› 2024, Vol. 45 ›› Issue (7): 127-134.doi: 10.7506/spkx1002-6630-20230818-120

• 营养卫生 • 上一篇    下一篇

榛蘑多糖对乙醇所致大鼠血管内皮细胞损伤的保护作用

张俊慧,陈然然,丛贺,沈明花   

  1. (延边大学医学院,吉林 延吉 133002)
  • 出版日期:2024-04-15 发布日期:2024-04-23
  • 基金资助:
    国家自然科学基金地区科学基金项目(81760031);吉林省中医药管理局中医药科技项目(2022094)

Protective Effects of Armillaria mellea Polysaccharides against Ethanol-Induced Vascular Endothelial Cell Injury in Rats

ZHANG Junhui, CHEN Ranran, CONG He, SHEN Minghua   

  1. (Medical College, Yanbian University, Yanji 133002, China)
  • Online:2024-04-15 Published:2024-04-23

摘要: 探究榛蘑多糖对乙醇所致大鼠血管内皮细胞损伤的保护作用。将40 只SD大鼠随机分成4 组(正常对照组、损伤组、榛蘑多糖低剂量组、榛蘑多糖高剂量组)。除正常对照组外的其余各组均按10 mL/kg mb灌胃体积分数40%乙醇诱导血管内皮细胞损伤。榛蘑多糖低、高剂量组分别以100、400 mg/kg mb灌胃榛蘑多糖,其余组以等体积生理盐水代替,实验共进行4 周。使用苏木精-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、诱导型一氧化氮合酶(inducible nitric oxide synthase,iNOS)、一氧化氮(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 μmol/mL乙醇诱导人脐静脉内皮细胞损伤模型,分析不同剂量(100、400 μg/mL)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,Bcl-2)、Bcl-2相关X蛋白(Bcl-2 associated X protein,Bax)和Caspase-3表达的影响。结果表明: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;在体外条件下,榛蘑多糖降低细胞ROS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Bcl-2/Bax,下调Cleaved caspase-3表达水平。综上,榛蘑多糖对乙醇诱导的大鼠血管内膜损伤有保护作用,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;血管内皮细胞损伤;乙醇;降脂;抗氧化

Abstract: The aim of this study is to evaluate the protective effect of Armillaria mellea polysaccharides (AMP) against ethanol-induced vascular endothelial cell injury in rats. Altogether 40 SD rats were randomly divided into 4 groups: normal control, injury, low- and high-dose AMP. The rats from all groups except the normal control group were gavaged with 40% ethanol at 10 mL/kg mb to induce endothelial cell injury. The rats in the low- and high-dose groups were gavaged with AMP at 100 and 400 mg/kg mb, respectively, while the remaining groups were given an equal volume of physiological saline. The administration period lasted for 4 weeks. The histopathological changes of carotid arteries were observed by hematoxylin-eosin (HE) staining. Serum 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, the effects of different doses (100 and 400 μg/mL) of AMP on the levels of reactive oxygen species (ROS), mitochondrial transmembrane potential, apoptosis, and the expression of apoptosis-associated proteins such as B cell lymphoma 2 (Bcl-2), Bcl-2 associated X protein (Bax), and caspase-3 in human umbilical vein endothelial cell injured by 600 μmol/mL ethanol were investigated. Results: AMP attenuated ethanol-induced endothelial cell injury, decreased T-CHO, TG, LDL-C, iNOS, NO, ET-1, and MDA levels, and increased HDL-C and SOD activity. In vitro, AMP reduced cellular ROS levels, inhibited the ethanol-induced decrease in mitochondrial transmembrane potential and apoptosis, increased Bcl-2/Bax ratio and down-regulated the expression of cleaved caspase-3. Conclusion: AMP have a protective effect against ethanol-induced endothelial cell 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 cell injury; ethanol; lipid-lowering; antioxidant

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