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异荭草素对油酸诱导的大鼠肝细胞氧化损伤和脂肪变性的保护作用

Protective Effect of Isoorientin on Oleic Acid-Induced Oxidative Damage and Steatosis in Rat Liver Cells.

作者信息

Luo Tongwang, Jiang Sheng, Zhou Bin, Song Quanjiang, Du Jing, Liu Ping, Wang Xiaodu, Song Houhui, Shao Chunyan

机构信息

Key Laboratory of Applied Technology on Green-Eco-Healthy Animal Husbandry of Zhejiang Province, Hangzhou, China.

Zhejiang Provincial Engineering Laboratory for Animal Health Inspection and Internet Technology, Hangzhou, China.

出版信息

Front Pharmacol. 2022 Feb 3;13:818159. doi: 10.3389/fphar.2022.818159. eCollection 2022.

DOI:10.3389/fphar.2022.818159
PMID:35185572
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8853441/
Abstract

The harm of nonalcoholic fatty liver disease to human health is increasing, which calls for urgent prevention and treatment of the disease. Isoorientin is an effective ingredient of Chinese herbal medicine with anti-inflammatory and antioxidant effects. However, the effect of isoorientin in nonalcoholic fatty liver disease is still unclear. In this study, combined and experiments, through pathological observation, flow cytometry, immunofluorescence and western blot analysis to explore the role of isoorientin in steatosis and reveal its molecular mechanism. The results demonstrated that oleic acid treatment significantly increased the content of ROS and lipid droplets in rat hepatocytes, and promoted the expression of γH2AX, HO-1, PPARγ, SREBP-1c, FAS. The ROS content in the cells of co-treated with isoorientin and oleic acid was significantly reduced compared to the oleic acid group, and the expression of γH2AX, HO-1, PPARγ, SREBP-1c, FAS, and the nuclear translocation of NF-κB p65 were also significantly inhibited. Our data showed that oleic acid induce oxidative damage and steatosis in hepatocytes both and , and activate the PPARγ/NF-κB p65 signal pathway. Moreover, isoorientin can significantly reduce oleic acid -induced oxidative damage and steatosis by regulating the PPARγ/NF-kB p65 signal pathway.

摘要

非酒精性脂肪性肝病对人类健康的危害日益增加,这就需要对该疾病进行紧急预防和治疗。异荭草素是一种具有抗炎和抗氧化作用的中草药有效成分。然而,异荭草素在非酒精性脂肪性肝病中的作用仍不明确。在本研究中,结合[具体实验名称1]和[具体实验名称2]实验,通过病理观察、流式细胞术、免疫荧光和蛋白质印迹分析,探讨异荭草素在脂肪变性中的作用并揭示其分子机制。结果表明,油酸处理显著增加了大鼠肝细胞中活性氧(ROS)和脂滴的含量,并促进了γH2AX、血红素加氧酶-1(HO-1)、过氧化物酶体增殖物激活受体γ(PPARγ)、固醇调节元件结合蛋白-1c(SREBP-1c)、脂肪酸合酶(FAS)的表达。与油酸组相比,异荭草素和油酸共同处理的细胞中ROS含量显著降低,γH2AX、HO-1、PPARγ、SREBP-1c、FAS的表达以及核因子κB p65(NF-κB p65)的核转位也受到显著抑制。我们的数据表明,油酸在体内和体外均诱导肝细胞氧化损伤和脂肪变性,并激活PPARγ/NF-κB p65信号通路。此外,异荭草素可通过调节PPARγ/NF-κB p65信号通路显著减轻油酸诱导的氧化损伤和脂肪变性。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2267/8853441/e54ff5dc5d23/fphar-13-818159-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2267/8853441/c9abee20d249/fphar-13-818159-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2267/8853441/82f71e35b8b6/fphar-13-818159-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2267/8853441/875ea391dae8/fphar-13-818159-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2267/8853441/4dcfb487063e/fphar-13-818159-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2267/8853441/9e89047e4b84/fphar-13-818159-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2267/8853441/e54ff5dc5d23/fphar-13-818159-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2267/8853441/c9abee20d249/fphar-13-818159-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2267/8853441/82f71e35b8b6/fphar-13-818159-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2267/8853441/875ea391dae8/fphar-13-818159-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2267/8853441/4dcfb487063e/fphar-13-818159-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2267/8853441/9e89047e4b84/fphar-13-818159-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2267/8853441/e54ff5dc5d23/fphar-13-818159-g006.jpg

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