食品科学 ›› 2025, Vol. 46 ›› Issue (21): 42-52.doi: 10.7506/spkx1002-6630-20250331-241

• 典型药食同源功能食品及其健康效应专栏 • 上一篇    

黄精多糖改善镉诱导大鼠胰腺损伤及其与肠道菌群和胰腺代谢的关联

阚玉娜,陈慧芳,高小娇,谢佳明,黄晓   

  1. (1.贵州中医药大学基础医学院,贵州?贵阳 550025;2.贵州中医药大学中医养生学院,贵州?贵阳 550025;3.贵州中医药大学第二附属医院,贵州?贵阳 550001)
  • 发布日期:2025-11-10
  • 基金资助:
    贵州省科技厅项目(黔科合基础-ZK[2021]一般497);贵州中医药大学学术新苗项目(贵科合学术新苗[2023]-35号)

Polygonatum sibiricum Polysaccharide Alleviates Cadmium-Induced Pancreatic Injury in Rats by Regulating the Gut Microbiota and Pancreatic Metabolism

KAN Yuna, CHEN Huifang, GAO Xiaojiao, XIE Jiaming, HUANG Xiao   

  1. (1. School of Basic Medical Medicine, Guizhou University of Traditional Chinese Medicine, Guiyang 550025, China; 2. Yangsheng College of Traditional Chinese Medicine, Guizhou University of Traditional Chinese Medicine, Guiyang 550025, China; 3. The Second Affiliated Hospital of Guizhou University of Traditional Chinese Medicine, Guiyang 550001, China)
  • Published:2025-11-10

摘要: 目的:探讨黄精多糖(Polygonatum sibiricum polysaccharide,PSP)对镉诱导大鼠胰腺损伤的拮抗效应及作用机制。方法:将24 只SPF级4 周龄雌性SD大鼠分为对照组(Con)、镉暴露组(Cd)和PSP干预组(Cd+PSP)。Cd组通过饮水暴露氯化镉(50 mg/L)建立模型,PSP干预组同时给予PSP灌胃(125 mg/(kg·d))。干预8 周后,检测体质量、空腹血糖(fasting blood glucose,FBG)、胰腺镉含量及组织病理变化,结合代谢组学和16S rRNA测序分析胰腺代谢物与肠道菌群的关联。结果:与Cd组相比,PSP干预组体质量显著增加(P<0.05),FBG和胰腺镉含量显著降低(P<0.05),苏木精-伊红染色显示,PSP缓解了镉诱导的胰岛萎缩和回肠绒毛结构损伤。代谢组学结果表明,PSP改善了镉暴露导致的氨基酸代谢(苯丙氨酸代谢)异常。肠道菌群分析表明,与Cd组相比,PSP提升了菌群α多样性(Chao1、Shannon指数)及β多样性,重建了益生菌互作网络并抑制致病菌(如Enterobacteriaceae)。结论:PSP对镉诱导的大鼠胰腺损伤有明显的缓解作用,其作用机制包括减少镉的蓄积、修复肠道屏障、改善胰腺代谢紊乱,以及调节肠道菌群平衡,本研究可为PSP相关功能产品的开发利用提供参考。

关键词: 黄精多糖;镉;胰腺;代谢组学;肠道菌群

Abstract: Objective: To investigate the alleviative effect and mechanism of Polygonatum sibiricum polysaccharide (PSP) on cadmium (Cd)-induced pancreatic injury in rats. Methods: Twenty-four SPF-grade four-week-old female Sprague Dawley (SD) rats were divided into three groups: control (Con), cadmium-exposed (Cd), and PSP intervention (Cd + PSP) groups. The rats from the Cd group were exposed to cadmium chloride (50 mg/L) via drinking water to establish a model of pancreatic injury, while those from the Cd + PSP group received Cd exposure and PSP gavage (125 mg/(kg·d)) concurrently. After eight weeks of intervention, body mass, fasting blood glucose (FBG), pancreatic cadmium content, and histopathological changes were measured. The association between pancreatic metabolites and the gut microbiota were analyzed using metabolomics and 16S rRNA sequencing. Results: Compared with the Cd group, the Cd + PSP group showed a significant increase in body mass (P < 0.05) and a significant reduction in FBG and pancreatic cadmium content (P < 0.05). Hematoxylin-eosin staining revealed that PSP alleviated Cd-induced pancreatic islet atrophy and structural damage to ileal villi. Metabolomic analysis demonstrated that PSP ameliorated Cd-induced abnormal amino acid metabolism (e.g., phenylalanine metabolism). Gut microbiota analysis indicated that PSP enhanced alpha diversity (Chao1 and Shannon index) and beta diversity, reconstructed the probiotic interaction network, and suppressed pathogenic bacteria (Enterobacteriaceae). Conclusion: PSP significantly mitigates Cd-induced pancreatic injury in rats through multiple mechanisms including reducing cadmium accumulation, repairing the intestinal barrier, improving pancreatic metabolic disorders, and regulating gut microbiota balance. This study provides a theoretical basis for developing PSP-based functional products.

Key words: Polygonatum sibiricum polysaccharide; cadmium; pancreas; metabolomics; gut microbiota

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