• 高脂饮食促进病毒性肝炎小鼠肝内细胞因子表达
  • 吴婷.高脂饮食促进病毒性肝炎小鼠肝内细胞因子表达[J].内科急危重症杂志,2023,29(3):236-241
    扫码阅读全文 本文二维码信息
    DOI:10.11768/nkjwzzzz20230315
    中文关键词:  高脂饮食  代谢异常  病毒性肝炎  细胞因子
    英文关键词:
    基金项目:湖北省自然科学基金面上项目 (No:2020CFB767); 同济医院优秀青年科学基金(No:2020YQ014)
    作者单位E-mail
    吴婷 华中科技大学同济医学院附属同济医院感染科 qning@vip.sina.com 
    摘要点击次数: 549
    全文下载次数: 899
    中文摘要:
          摘要 目的:研究高脂饮食对病毒性肝炎小鼠肝内细胞因子表达的影响。方法:选取C3H/HeN小鼠共152只,随机分为标准饮食组(32只)、高脂饮食组(32只)、标准饮食感染组(44只)、高脂饮食感染组(44只)。标准饮食组及标准饮食感染组持续予以标准饮食喂养,高脂饮食组及高脂饮食感染组持续予以高脂饮食喂养。喂养第12周末,标准饮食感染组及高脂饮食感染组予以腹腔注射3型鼠肝炎病毒(MHV-3)诱导病毒性肝炎。于感染后不同时间点,采用定量逆转录聚合酶链式反应(PCR)检测肝内肿瘤坏死因子(TNF-α)、白介素(IL)-1β、IL-6、IL-17A表达。结果:高脂饮食喂养12周诱导小鼠出现代谢异常。感染后第4天,标准饮食感染组小鼠肝内仅IL-6表达上调,而高脂饮食感染组TNF-α、IL-1β、IL-6、IL-17A表达上调(P均<0.05)。感染后第8天,标准饮食感染组及高脂饮食感染组小鼠肝内TNF-α、IL-1β、IL-6、IL-17A表达上调,且高脂饮食感染组表达水平显著高于标准饮食感染组(P均<0.05)。感染后第12天,标准饮食感染组小鼠肝内TNF-α、IL-17A表达回落至未感染水平,高脂饮食感染组仅IL-6表达回落。感染后第16天,标准饮食感染组小鼠肝内炎性细胞因子表达均回落至未感染水平,高脂饮食感染组仅IL-1β、IL-6表达回落。结论:高脂饮食促使病毒性肝炎小鼠肝内炎性细胞因子表达上调出现更早、幅度更高、持续更久。
    英文摘要:
          Abstract Objective: To investigate the effect of high-fat diet on the expression of inflammatory cytokines in viral hepatitis mouse model. Methods: Totally, 152 C3H/HeN mice were allocated to standard diet group (n=32), high-fat diet group (n=32), standard diet with infection group (n=44), and high-fat diet with infection group (n=44). The standard diet group and standard diet with infection group were treated with standard diet throughout the study; the high-fat diet group and high-fat diet with infection group were treated with high-fat diet throughout the study. The standard diet with infection group and high-fat diet with infection group were infected with murine hepatitis virus 3 (MHV-3) after 12-week feeding. The expression of intrahepatic TNF-α, IL-1β, IL-6 and IL-17A was detected using quantitative reverse transcription polymerase chain reaction at different time points post-infection. Results: The 12-week high-fat diet feeding induced metabolic abnormalities in mice. At day 4 post-infection, only the intrahepatic expression of IL-6 increased in standard diet with infection mice, while the expression of TNF-α, IL-1β, IL-6 and IL-17A increased in high-fat diet with infection group (P<0.05). At day 8 post-infection, the intrahepatic expression of TNF-α, IL-1β, IL-6 and IL-17A was elevated in both two infected groups, and was significantly higher in high-fat diet with infection group (P< 0.05). At day 12 post-infection, the intrahepatic expression of TNF-α and IL-17A in standard diet with infection group and IL-6 in high-fat diet with infection group fell back to baseline. At day 16 post-infection, intrahepatic expression of these cytokines was not upregulated in standard diet with infection group, while the expression of IL-1β and IL-6 in high-fat diet with infection group fell back to baseline. Conclusion: High-fat diet feeding promoted an early-onset, enhanced and prolonged hepatitis virus-induced upregulation of intrahepatic inflammatory cytokines expression.