四川农业大学学报 ›› 2020, Vol. 38 ›› Issue (03): 319-325.doi: 10.16036/j.issn.1000-2650.2020.03.010

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染料木素对高脂诱导肥胖小鼠肝脏炎症及脂联素信号通路的影响

王书杰1, 甘麦邻1, 沈林園1, 杨东丽2, 唐国庆1, 张顺华1, 朱砺1,*   

  1. 1.四川农业大学动物科技学院/畜禽遗传资源发掘与创新利用四川省重点实验室,成都 611130;
    2.泸州市农业农村局,四川 泸州 646000
  • 收稿日期:2020-02-15 出版日期:2020-06-28 发布日期:2021-02-03
  • 作者简介:王书杰,硕士研究生。*责任作者:朱砺,教授,博士生导师,主要从事猪遗传育种研究,E-mail:zhuli7508@163.com。
  • 基金资助:
    国家重点研发计划项目(2018YFD0501004); 四川省科技支撑项目(2016NYZ0050,SCSZTD-3-008)

Effects of Genistein on Liver Inflammation and Adiponectin Signaling Pathway in Obese Mice Induced by High-Fat Diet

WANG Shujie1, GAN Mailin1, SHEN Linyuan1, YANG Dongli2, TANG Guoqing1, ZHANG Shunhua1, ZHU li1,*   

  1. 1. College of Animal Science and Technology/Farm Animal Genetic Resources Exploration and Innovation Key Laboratory of Sichuan Province,Sichuan Agricultural University,Chengdu 611130,China;
    2. Luzhou Agricultural and Rural Bureau,Luzhou 646000,Sichuan,China
  • Received:2020-02-15 Online:2020-06-28 Published:2021-02-03

摘要: 【目的】探讨染料木素对高脂饮食导致肥胖小鼠肝脏的治疗作用及其潜在机制。【方法】30只ICR雌性肥胖小鼠随机分为对照组(ND)、高脂组(HFD)和高脂染料木素组(HFD-G),每组各10只。对照组饲以普通饲料,高脂组饲以高脂饲料,高脂染料木素组饲以高脂-染料木素预混料。干预14周后测量小鼠肝脏重量、葡萄糖耐受情况,通过甘油三酯、总胆固醇测定试剂盒检测小鼠血清中甘油三酯(triglyceride,TG)、总胆固醇(total cholesterol,TC)含量;通过油红O染色观察肝脏的组织形态和脂滴沉积情况;qRT-PCR检测肝脏组织中炎症因子肿瘤坏死因子α (tumor necrosis factor-α,TNF-α)、白细胞介素-6(interleukin-6,IL-6)、脂联素(adiponectin,ADPN)、脂联素受体-1(adiponectin receptor 1,AdipoR1)以及脂联素受体-2(adiponectin receptor 2,AdipoR2) mRNA表达水平;ELISA法检测血清中TNF-α和IL-6的表达。【结果】饲喂14周后,高脂组体重、肝重显著高于对照组(P<0.05),血清中的TG、TC含量极显著高于对照组(P<0.01),ADPNAdipoR1AdipoR2的mRNA表达水平显著低于对照组(P<0.05),炎症因子TNF-αIL-6的mRNA表达水平以及ELISA结果显著高于对照组(P<0.05),油红O染色结果显示,高脂组较对照组肝脏的脂质沉积情况显著加重(P<0.05);高脂染料木素组体重、肝重显著低于高脂组(P<0.05),血清中的TG、TC含量极显著低于高脂组(P<0.01),ADPNAdipoR1AdipoR2的mRNA表达水平显著高于高脂组(P<0.05),炎症因子TNF-αIL-6的mRNA表达水平以及细胞因子分泌水平显著低于高脂组(P<0.05),油红O染色结果显示,高脂染料木素组较高脂组肝脏的脂质沉积情况显著减轻(P<0.05)。【结论】染料木素能够显著缓解由高脂饮食引起的肝脏病变,其机制可能是通过提高脂联素表达水平同时抑制肝脏中的炎性因子来实现的。

关键词: 染料木素, 肥胖, 肝脏, 炎症, 脂联素

Abstract: 【Objective】 This study was performed to investigate the effect of genisteinon obese mouse liver caused by high-fat diet. 【Method】 Female ICR mice (n=30) were divided randomly into control (ND) group, high fat diet (HFD) group, and high-fat genistein (HFD-G) group, with 10 mice in each group. The ND group was fed with ordinary feed, the HFD group was fed with high fat feed, and the HFD-G group was fed with high fat-genistein premix feed. After intervention with genistein, the mouse liver weight, triglyceride (TG) and total cholesterol (TC) in the serum were measured. Oil red O staining was used to observe tissue morphology and lipid droplet deposition; qRT-PCR was used to detect mRNA expression levels of inflammatory factors tumor necrosis factor α (TNF-α), interleukin-6 (IL-6), and adiponectin (ADPN), adiponectin receptor-1 (AdipoR1) and adiponectin receptor-2 (AdipoR2) in liver tissues. ELISA was applied to detect the expression levels of TNF-α and IL-6 in serum. 【Result】 After 14 weeks, body and liver weight of HFD group were significantly higher than the control group (P<0.05). TC and TG of HFD group were extremely significantly higher than the control group (P<0.01). The mRNA expression levels of ADPN, AdipoR1 and AdipoR2 in HFD group were significantly lower than that in the ND group (P<0.05). The mRNA expression levels of inflammatory factors TNF-α and IL-6 in HFD group were significantly higher than those in the ND group (P<0.05). Oil red O staining results showed that the lipid deposition in the HFD group was significantly thicker than that in the NC group (P<0.05); body and liver weight of HFD-G group were significantly lower than that in the HFD group (P<0.05), TC and TG of HFD-G group were extremely significantly higher than that in the HFD group (P<0.01). The mRNA expression levels of ADPN, AdipoR1 and AdipoR2 in HFD-G group were significantly higher than that in the HFD group (P<0.05), mRNA expression levels of inflammatory factors TNF-α, IL-6 and cytokine secretion level results were significantly lower than that in the HFD group (P<0.05). Oil red O staining results showed that the lipid deposition in HFD-G group was significantly reduced than that in the HFD group (P<0.05). 【Conclusion】 Genistein could significantly relieve liver disease caused by high-fat diet. The mechanism may be due to that genistein could increase the expression level of adiponectin and suppressed the expression levels of inflammatory factors in the liver.

Key words: genistein, fat, liver, inflammation, adiponectin

中图分类号: 

  • TS201.4