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

Dietary Beta-Hydroxy Beta-Methyl Butyrate Supplementation Alleviates Liver Injury in Lipopolysaccharide-Challenged Piglets.
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日粮补充 β-羟基 β-甲基丁酸酯可减轻脂多糖挑战仔猪的肝损伤

DOI:
10.1155/2021/5546843
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发表时间:
2021
影响因子:
--
通讯作者:
Li F
Li F
中科院分区:
生物学2区
文献类型:
--
作者:
Duan Y;Song B;Zheng C;Zhong Y;Guo Q;Zheng J;Yin Y;Li J;Li F

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本研究旨在探讨β-羟基-β-甲基丁酸(HMB)对脂多糖(LPS)诱导的仔猪肝损伤的影响及其机制。30头(21 ± 2日龄,体重5.86 ± 0.18 kg)仔猪随机分为对照组(基础日粮,注射生理盐水)、LPS组(基础日粮)和LPS + HMB组(基础日粮+0.60% HMB-Ca)。在用LPS和/或HMB处理15天后,获得血液和肝脏样品。结果表明,在LPS注射仔猪中,补充HMB可改善LPS攻击诱导的肝脏组织形态学异常。与对照组相比,注射LPS的仔猪血清天冬氨酸转氨酶和碱性磷酸酶活性显著升高(P <0.05)。LPS刺激后L-PFK、ACO、L-CPT-1、ICDH β和AMPK α 1/2的mRNA表达下调,PCNA、caspase 3、TNF-α、TLR 4、MyD 88、NOD 1和NF-κ B p65的mRNA表达上调(P <0.05)。然而,这些不利影响的LPS攻击被逆转HMB补充(P <0.05)。提示HMB对LPS诱导的肝损伤具有保护作用,其机制可能是通过调节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反应。
The current study was performed to investigate whether dietary β-hydroxy-β-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 (P < 0.05). The LPS challenge also downregulated the mRNA expression of L-PFK, ACO, L-CPT-1, ICDH β, and AMPKα1/2 and upregulated the mRNA expression of PCNA, caspase 3, TNF-α, TLR4, MyD88, NOD1, and NF-κB p65 (P < 0.05). However, these adverse effects of the LPS challenge were reversed by HMB supplementation (P < 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.
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