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饲粮添加β-羟基-β-甲基丁酸盐缓解脂多糖应激仔猪的肝损伤。

Dietary Beta-Hydroxy Beta-Methyl Butyrate Supplementation Alleviates Liver Injury in Lipopolysaccharide-Challenged Piglets.

机构信息

CAS Key Laboratory of Agro-ecological Processes in Subtropical Region, Hunan Provincial Key Laboratory of Animal Nutritional Physiology and Metabolic Process, National Engineering Laboratory for Pollution Control and Waste Utilization in Livestock and Poultry Production, Institute of Subtropical Agriculture, Chinese Academy of Sciences, Changsha 410125, China.

University of Chinese Academy of Sciences, Beijing 100039, China.

出版信息

Oxid Med Cell Longev. 2021 Apr 1;2021:5546843. doi: 10.1155/2021/5546843. eCollection 2021.

DOI:10.1155/2021/5546843
PMID:33868570
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8035022/
Abstract

The current study was performed to investigate whether dietary -hydroxy--methylbutyrate (HMB) could regulate liver injury in a lipopolysaccharide- (LPS-) challenged piglet model and to determine the mechanisms involved. Thirty piglets (21 ± 2 days old, 5.86 ± 0.18 kg body weight) were randomly divided into the control (a basal diet, saline injection), LPS (a basal diet), or LPS+HMB (a basal diet + 0.60% HMB-Ca) group. After 15 d of treatment with LPS and/or HMB, blood and liver samples were obtained. The results showed that in LPS-injected piglets, HMB supplementation ameliorated liver histomorphological abnormalities induced by LPS challenge. Compared to the control group, the activities of serum aspartate aminotransferase and alkaline phosphatase were increased in the LPS-injected piglets ( < 0.05). The LPS challenge also downregulated the mRNA expression of L-PFK, ACO, L-CPT-1, ICDH , and AMPK1/2 and upregulated the mRNA expression of PCNA, caspase 3, TNF-, TLR4, MyD88, NOD1, and NF-B p65 ( < 0.05). However, these adverse effects of the LPS challenge were reversed by HMB supplementation ( < 0.05). These results indicate that HMB may exert protective effects against LPS-induced liver injury, and the underlying mechanisms might involve the improvement of hepatic energy metabolism via regulating AMPK signaling pathway and the reduction of liver inflammation via modulating TLR4 and NOD signaling pathways.

摘要

本研究旨在探讨饲粮中补充β-羟基-β-甲基丁酸(HMB)是否能缓解脂多糖(LPS)刺激仔猪的肝损伤,并确定相关机制。30 头 21±2 日龄、5.86±0.18kg 体重的仔猪随机分为对照组(基础饲粮,生理盐水注射)、LPS 组(基础饲粮,LPS 注射)和 LPS+HMB 组(基础饲粮+0.60% HMB-Ca)。用 LPS 和/或 HMB 处理 15d 后,采集血液和肝脏样本。结果表明,在 LPS 注射仔猪中,HMB 补充改善了 LPS 刺激引起的肝脏组织形态学异常。与对照组相比,LPS 注射仔猪血清天冬氨酸转氨酶和碱性磷酸酶活性升高(<0.05)。LPS 刺激还下调了 L-PFK、ACO、L-CPT-1、ICDH 和 AMPK1/2 的 mRNA 表达,上调了 PCNA、caspase 3、TNF-α、TLR4、MyD88、NOD1 和 NF-κB p65 的 mRNA 表达(<0.05)。然而,HMB 补充缓解了 LPS 刺激的这些不利影响(<0.05)。这些结果表明,HMB 可能对 LPS 诱导的肝损伤具有保护作用,其作用机制可能涉及通过调节 AMPK 信号通路改善肝脏能量代谢,通过调节 TLR4 和 NOD 信号通路减轻肝脏炎症。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/958d/8035022/3f36cddff247/OMCL2021-5546843.007.jpg
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