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臭氧暴露对 Huh-7 人肝癌细胞脂质代谢的影响。

Effects of ozone exposure on lipid metabolism in Huh-7 human hepatoma cells.

机构信息

College of Animal Science and Technology, Inner Mongolia University for Nationalities, Tongliao, China.

Department of Orthopedic Trauma, Beijing Jishuitan Hospital, Beijing, China.

出版信息

Front Public Health. 2023 Jul 13;11:1222762. doi: 10.3389/fpubh.2023.1222762. eCollection 2023.

Abstract

Ozone pollution is a major environmental concern. According to recent epidemiological studies, ozone exposure increases the risk of metabolic liver disease. However, studies on the mechanisms underlying the effects of ozone exposure on hepatic oxidative damage, lipid synthesis, and catabolism are limited. In this study, Huh-7 human hepatocellular carcinoma cells were randomly divided into five groups and exposed to 200 ppb O for 0, 1, 2, 4, and 8 h. We measured the levels of oxidative stress and analyzed the changes in molecules related to lipid metabolism. The levels of oxidative stress were found to be significantly elevated in Huh-7 hepatocellular carcinoma cells after O exposure. Moreover, the expression levels of intracellular lipid synthases, including SREBP1, FASN, SCD1, and ACC1, were enhanced. Lipolytic enzymes, including ATGL and HSL, and the mitochondrial fatty acid oxidase, CPT1α, were inhibited after O exposure. In addition, short O exposure enhanced the expression of the intracellular peroxisomal fatty acid β-oxidase, ACOX1; however, its expression decreased adaptively with longer exposure times. Overall, O exposure induces an increase in intracellular oxidative stress and disrupts the normal metabolism of lipids in hepatocytes, leading to intracellular lipid accumulation.

摘要

臭氧污染是一个主要的环境问题。根据最近的流行病学研究,臭氧暴露会增加代谢性肝病的风险。然而,关于臭氧暴露对肝氧化损伤、脂质合成和分解代谢影响的机制研究有限。在这项研究中,Huh-7 人肝癌细胞被随机分为五组,分别暴露于 200 ppb 的臭氧中 0、1、2、4 和 8 小时。我们测量了氧化应激水平,并分析了与脂质代谢相关的分子变化。结果发现,臭氧暴露后 Huh-7 肝癌细胞的氧化应激水平显著升高。此外,细胞内脂质合成酶的表达水平,包括 SREBP1、FASN、SCD1 和 ACC1,也增强了。脂解酶,包括 ATGL 和 HSL,以及线粒体脂肪酸氧化酶 CPT1α,在臭氧暴露后受到抑制。此外,短时间的臭氧暴露会增强细胞内过氧化物酶体脂肪酸β-氧化酶 ACOX1 的表达;然而,随着暴露时间的延长,其表达会适应性下降。总的来说,臭氧暴露会导致细胞内氧化应激增加,并破坏肝细胞内脂质的正常代谢,导致细胞内脂质堆积。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/96fb/10374329/b0798db45f86/fpubh-11-1222762-g001.jpg

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