研究报告

脱镁叶绿酸a缓解高脂膳食诱导的小鼠肝肠损伤研究

  • 刘若曦 ,
  • 曾全恒 ,
  • 蔡甜 ,
  • 陈科伟
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  • 1(西南大学 食品科学学院, 重庆, 400715)
    2(西南大学 食品科学与工程国家级实验教学示范中心, 重庆, 400715)
    3(西南大学 化学化工学院, 重庆, 400715)
    4(西南大学 中匈食品科学合作中心, 重庆, 400715)
    5(川渝共建特色食品重庆市重点实验室, 重庆, 400715)
    6(农业农村部农产品贮藏保鲜质量安全风险评估实验室(重庆), 重庆, 400715)
第一作者:本科生(陈科伟副教授为通信作者,E-mail:chenkewei@swu.edu.cn)

收稿日期: 2024-06-30

  修回日期: 2024-08-07

  网络出版日期: 2025-06-11

基金资助

国家重点研发计划(2023YFE0116100);重庆市科委基础研究与前沿探索项目(自然科学基金CSTB2022NSCQ-MSX0633);西南大学创新研究2035先导计划重点项目(SWU-XDZD22007)

Studies on alleviation of high-fat diet-induced liver and intestinal damage by pheophorbide a

  • LIU Ruoxi ,
  • ZENG Quanheng ,
  • CAI Tian ,
  • CHEN Kewei
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  • 1(College of Food Science, Southwest University, Chongqing 400715, China)
    2(National Demonstration Center for Experimental Food Science and Technology Education, Southwest University, Chongqing 400715, China)
    3(School of Chemistry and Chemical Engineering, Southwest University, Chongqing 400715, China)
    4(China-Hungary Cooperative Center for Food Science, Southwest University, Chongqing 400715, China)
    5(Chongqing Key Laboratory of Speciality Food Co-Built by Sichuan and Chongqing, Chongqing 400715, China)
    6(Laboratory of Quality & Safety Risk Assessment for Agro-products on Storage and Preservation (Chongqing), Ministry of Agriculture and Rural Affairs of the People’s Republic of China, Chongqing 400715, China)

Received date: 2024-06-30

  Revised date: 2024-08-07

  Online published: 2025-06-11

摘要

该文结合组织病理、血液生化及高通量分析技术(微生物多样性和肝、菌群代谢组学)研究不同质量浓度(0.16、0.12、0.08、0.04 mg/mL)脱镁叶绿酸a(pheophorbide a,Pheo a)对高脂膳食诱导的小鼠肝肠损伤的缓解作用及机制。体重结果表明高浓度组(0.16、0.12 mg/mL)小鼠体重显著低于高脂膳食对照组(P<0.05)。血糖值测定结果发现高浓度组小鼠血糖值处于正常范围,而低浓度组(0.08、0.04 mg/mL)和高脂膳食对照组处于糖尿病前期血糖值范围。血清指标检测结果显示脱镁叶绿酸a显著降低高脂膳食诱导的甘油三酯、胰岛素、IL-6、IL-1β、丙二醛表达水平(P<0.05),且呈剂量依赖关系。肝脏代谢组学结果表明烟酰甘氨酸、琥珀酸、丙氨酸、谷氨酸和缬氨酸等代谢物发生显著变化(P<0.05)。微生物多样性结果显示脱镁叶绿酸a在属水平上显著升高拟杆菌属(Muribaculaceae)和乳杆菌属(Lactobacillus)的丰度,降低梭菌属(Clostridium)的丰度(P<0.05)。肠道菌群代谢组学揭示草乙酸、甲基-2-羟基异丁酸、α-酮戊二酸等代谢物发生显著变化(P<0.05)。综上,脱镁叶绿酸a可有效延缓高脂膳食小鼠体重增加,对小鼠肠道菌群具有调节作用,显著逆转高脂膳食诱导的肠道菌群失调,并减少高脂膳食引起的低度炎症,进而缓解代谢综合征、促进机体健康,相应的调控机制还需深入研究。

本文引用格式

刘若曦 , 曾全恒 , 蔡甜 , 陈科伟 . 脱镁叶绿酸a缓解高脂膳食诱导的小鼠肝肠损伤研究[J]. 食品与发酵工业, 2025 , 51(10) : 77 -87 . DOI: 10.13995/j.cnki.11-1802/ts.040344

Abstract

This paper combined histopathology, blood biochemistry, and high-throughput analytical techniques (microbial diversity and metabolomics of liver and flora) to study the mitigating effect and mechanism of different concentrations (0.16, 0.12, 0.08, 0.04 mg/mL) of pheophorbide a (Pheo a) on the liver and intestinal damage induced by high-fat diet.Body weight results showed that the body weight of mice in the high-concentration group (0.16, 0.12 mg/mL) was significantly lower than that of the high-fat dietary control group (P<0.05).Blood glucose values were measured and found to be in the normal range in the high-concentration group, while the low-concentration group (0.08, 0.04 mg/mL) and the high-fat dietary control group were in the range of pre-diabetic blood glucose values.The results of serum indexes showed that pheophorbide a significantly reduced the high-fat diet-induced triglyceride, insulin, IL-6, IL-1β, and malondialdehyde expression levels (P<0.05) in a dose-dependent manner.Liver metabolomics results showed significant changes in metabolites of nicotinoylglycine, succinic acid, alanine, glutamic acid, and valine (P<0.05).Microbial diversity results revealed that the experimental group significantly increased the abundance of Muribaculaceae and Lactobacillus and decreased the abundance of Clostridium at the genus level (P<0.05).Metabolomics of intestinal flora revealed significant changed in metabolites such as oxalacetic acid, methyl-2-hydroxyisobutyric acid, and α-ketoglutaric acid (P<0.05).In conclusion, pheophorbide a could effectively delay weight gain and have a regulatory effect on the intestinal flora of mice, significantly reversing high-fat diet-induced intestinal flora dysbiosis and reducing high-fat diet-induced low-grade inflammation, which in turn alleviates the metabolic syndrome and promotes the health of the organism, and the corresponding regulatory mechanisms need to be studied in depth.

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