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三价铬补充剂可改善油酸诱导的小鼠肝脂肪变性。

Trivalent Chromium Supplementation Ameliorates Oleic Acid-Induced Hepatic Steatosis in Mice.

机构信息

State Key Laboratory of Bioreactor Engineering, East China University of Science and Technology, 130 Meilong Road, Shanghai, 200237, China.

Shanghai Key Laboratory of Crime Scene Evidence, Shanghai Research Institute of Criminal Science and Technology, Zhongshan North No 1 Road, Shanghai, 200083, China.

出版信息

Biol Trace Elem Res. 2019 Jan;187(1):192-201. doi: 10.1007/s12011-018-1368-0. Epub 2018 May 24.

Abstract

Trivalent chromium [Cr(III)] is recognized as an essential trace element for human health, whereas its effect on hepatic lipid metabolism has not yet been fully understood. This study aimed to investigate the beneficial effects and potential mechanisms of Cr(III) on hepatic steatosis in an oleic acid (OA) induced mice model. Mice were fed with high OA for 12 weeks to induce lipid accumulation, and co-administrated with Cr(III) supplementation. Indexes of liver lipid accumulation, associated lipid genes expression, fatty acids (FAs) profile and inflammatory cytokines were analyzed. The data showed that Cr(III) supplementation could attenuate disease progress of hepatic steatosis and protect liver from high OA. After Cr(III) supplementation, elevated body weight and liver injury in steatosis mice were reversed, excessive lipid accumulation and FAs were also reduced. The up-regulation of cluster of differentiation 36 (CD36) and diacylglycerol acyltransferase 2 (DGAT2) following steatosis induction were inhibited by Cr(III). Cr(III) reduced the content of pro-inflammatory cytokines (IL-1β and TNF-α, IL-12) and restored the level of anti-inflammatory cytokine (IL-10) to the control values. Our results suggest that Cr(III) supplementation is a novel strategy for alleviating OA-induced hepatic steatosis.

摘要

三价铬[Cr(III)]被认为是人体健康所必需的微量元素,但其对肝脏脂质代谢的影响尚未完全阐明。本研究旨在探讨三价铬(Cr(III))对油酸(OA)诱导的小鼠模型肝脂肪变性的有益作用及其潜在机制。用高 OA 喂养小鼠 12 周以诱导脂质积累,并同时给予 Cr(III)补充。分析了肝脏脂质积累的指标、相关脂质基因表达、脂肪酸(FA)谱和炎症细胞因子。结果表明,Cr(III)补充可减轻肝脂肪变性的疾病进展并保护肝脏免受高 OA 的影响。Cr(III)补充后,脂肪变性小鼠的体重升高和肝损伤得到逆转,过量的脂质积累和 FA 也减少。Cr(III)抑制了脂肪变性诱导后 CD36 和二酰基甘油酰基转移酶 2(DGAT2)的上调。Cr(III)降低了促炎细胞因子(IL-1β和 TNF-α、IL-12)的含量,并将抗炎细胞因子(IL-10)的水平恢复到对照值。我们的结果表明,Cr(III)补充是一种缓解 OA 诱导的肝脂肪变性的新策略。

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