水飞蓟素介导肠-肝轴通路,缓解碳酸盐暴露引起的鲫鱼肝脏脂质代谢紊乱

IF 2.2 2区 生物学 Q4 BIOCHEMISTRY & MOLECULAR BIOLOGY
Xin-yu Lei, Xin Wang, Xue Cao, Yue-hong Li
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引用次数: 0

摘要

为了研究水飞蓟素缓解河坊鲫鱼(13.43 ± 0.059 g)因碳酸盐暴露引起的肝脏脂质代谢异常的机制,我们进行了为期 8 周的喂养试验。将鱼随机分为三组:对照组(B组,0 g/L碳酸盐,0 mg/kg水飞蓟素)、碳酸盐胁迫组(CA组,3 g/L碳酸盐,0 mg/kg水飞蓟素)和水飞蓟素组(SI组,3 g/L碳酸盐,60 mg/kg水飞蓟素)。与 CA 组相比,SI 组刷状绒毛明显恢复,粘膜下宽度减少。与 B 组相比,CA 组肠道屏障受损,通透性增加,而 SI 组受损情况减轻。肠道微生物群分析表明,CA组与脂多糖生物合成蛋白和脂多糖生物合成相关的细菌群落功能基因高于B组和SI组,发现鱼体内LPS含量的变化与肠道微生物群的结果相呼应。与 B 组相比,CA 组肝脏受损,脂质代谢过程异常,导致脂质代谢紊乱。SI 组缓解了碳酸盐暴露对肝脏的损伤,促进了肝脏脂质合成过程,平衡了机体脂质代谢。50%以上的代谢物与脂质和脂质分子密切相关。代谢物中最多的是氧化磷酸化和丙酮酸代谢。综上所述,本研究证明水飞蓟素缓解碳酸盐暴露改变了HCC患者肠道微生物群平衡,导致肠道炎症和黏膜屏障通透性增加,抑制LPS合成和吸收,阻止其通过肠肝进入肝脏,增加肝脏氧化应激和肝脏脂质代谢异常,从而导致肝损伤。为水飞蓟素功能性饲料添加剂的开发利用和碳酸盐暴露对鱼类肝损伤的缓解策略提供理论依据。
本文章由计算机程序翻译,如有差异,请以英文原文为准。

Silymarin mediates the gut-liver axis pathway to alleviate Carassius auratus hepatic lipid metabolism disorders caused by carbonate exposure

Silymarin mediates the gut-liver axis pathway to alleviate Carassius auratus hepatic lipid metabolism disorders caused by carbonate exposure
An 8-week feeding trial was conducted to investigate the mechanism of silymarin alleviating the abnormal lipid metabolism of Hefang Crucian Carp (HCC) (13.43 ± 0.059 g) liver caused by carbonate exposure. The fish were randomly divided into three groups: Control group (group B, 0 g/L carbonate, 0 mg/kg silymarin), carbonate stress group (group CA, 3 g/L carbonate, 0 mg/kg silymarin) and silymarin group (group SI, 3 g/L carbonate, 60 mg/kg silymarin). The results showed that the growth performance of group CA was significantly increased compared with group B. Compared with CA group, brush villi in SI group recovered significantly, and the width of submucosa decreased. Compared with group B, the intestinal barrier was damaged and permeability increased in group CA, while the damage was alleviated in group SI. Intestinal microbiota analysis showed that the bacterial community function genes related to lipopolysaccharide biosynthesis protein and lipopolysaccharide biosynthesis in CA group were higher than those in B and SI groups, and it was found that the change of LPS content in fish was echoed by the results of intestinal microflora. Compared with group B, the liver of group CA was damaged and the lipid metabolism process was abnormal, resulting in lipid metabolism disorder. SI group alleviated the liver damage caused by carbonate exposure, promoted the process of liver lipid synthesis, and balanced the body's lipid metabolism. More than 50 % of the metabolites are closely related to lipids and lipid molecules. The most metabolites in metabolism are oxidative phosphorylation and pyruvate metabolism. In summary, this study demonstrated that silymarin alleviating carbonate exposure altered intestinal microbiota homeostasis in HCC, leading to intestinal inflammation and increased mucosal barrier permeability, inhibiting LPS synthesis and absorption, preventing it from entering the liver through the intestinal liver, and increasing oxidative stress in the liver and abnormal lipid metabolism in the liver, thereby leading to liver injury. To provide theoretical basis for the development and utilization of silymarin functional feed additives and the mitigation strategy of carbonate exposure to liver damage in fish.
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来源期刊
CiteScore
5.10
自引率
3.30%
发文量
69
审稿时长
33 days
期刊介绍: Comparative Biochemistry & Physiology (CBP) publishes papers in comparative, environmental and evolutionary physiology. Part D: Genomics and Proteomics (CBPD), focuses on “omics” approaches to physiology, including comparative and functional genomics, metagenomics, transcriptomics, proteomics, metabolomics, and lipidomics. Most studies employ “omics” and/or system biology to test specific hypotheses about molecular and biochemical mechanisms underlying physiological responses to the environment. We encourage papers that address fundamental questions in comparative physiology and biochemistry rather than studies with a focus that is purely technical, methodological or descriptive in nature.
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