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Turcz. 根中游离酚类物质对四氯化碳诱导的肝损伤的保护作用以及……(原文此处不完整)

Protective effect of free phenolics from Turcz. root on carbon tetrachloride-induced liver injury and .

作者信息

Lu Yue-Hong, Tian Cheng-Rui, Gao Chun-Yan, Wang Wen-Jing, Yang Wen-Yi, Kong Xiao, Chen You-Xia, Liu Zhen-Zhen

机构信息

College of Food Engineering and Nutritional Science, Shaanxi Normal University, Xi'an, China.

College of Agronomy and Biological Science, Dali University, Dali, China.

出版信息

Food Nutr Res. 2018 Jul 25;62. doi: 10.29219/fnr.v62.1398. eCollection 2018.

DOI:10.29219/fnr.v62.1398
PMID:30083087
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6064781/
Abstract

Protective effect of free phenolics from Turcz. root (FPLR) on CCl-induced hepatotoxicity and was first evaluated. Oral administration of FPLR (100 mg/kg bw) to mice significantly reduced the CCl-induced elevation of serum alanine aminotransferase, aspartate aminotransferase, alkaline phosphatase, triacylglycerols, total cholesterol, and total bilirubin. FPLR also increased the hepatic GSH contents and antioxidant enzyme activities of SOD and CAT and decreased the hepatic MDA level. Histopathological examinations further confirmed that the FPLR could protect the liver from CCl-induced damage. Further research indicated that FPLR prevented the DNA fragmentation caused by CCl based on TUNEL assay. Moreover, immunohistochemistry staining demonstrated that pretreatment with FPLR significantly inhibited the elevation of hepatic TNF-α, IL-6, IL-8, iNOS, COX-2, and Caspase-3 in CCl-treated mice. experiments showed that FPLR remarkably reduced BRL hepatocyte apoptosis and damage caused by CCl treatment. These findings indicate that FPLR could be developed as a functional food or medication for therapeutic purpose and prevention of hepatic injury.

摘要

首次评估了地锦草根中游离酚类物质(FPLR)对四氯化碳诱导的肝毒性的保护作用。给小鼠口服FPLR(100毫克/千克体重)可显著降低四氯化碳诱导的血清丙氨酸氨基转移酶、天冬氨酸氨基转移酶、碱性磷酸酶、三酰甘油、总胆固醇和总胆红素的升高。FPLR还增加了肝脏中谷胱甘肽(GSH)含量以及超氧化物歧化酶(SOD)和过氧化氢酶(CAT)的抗氧化酶活性,并降低了肝脏丙二醛(MDA)水平。组织病理学检查进一步证实FPLR可保护肝脏免受四氯化碳诱导的损伤。进一步研究表明,基于TUNEL检测,FPLR可防止四氯化碳引起的DNA片段化。此外,免疫组织化学染色表明,FPLR预处理可显著抑制四氯化碳处理小鼠肝脏中肿瘤坏死因子-α(TNF-α)、白细胞介素-6(IL-6)、白细胞介素-8(IL-8)、诱导型一氧化氮合酶(iNOS)、环氧化酶-2(COX-2)和半胱天冬酶-3(Caspase-3)的升高。实验表明,FPLR可显著减少四氯化碳处理引起的BRL肝细胞凋亡和损伤。这些发现表明,FPLR可开发成为用于治疗目的和预防肝损伤的功能性食品或药物。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2b85/6064781/2511a7465ac8/FNR-62-1398-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2b85/6064781/d63ac87048eb/FNR-62-1398-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2b85/6064781/3827a943a69f/FNR-62-1398-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2b85/6064781/5d1773aefe18/FNR-62-1398-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2b85/6064781/2511a7465ac8/FNR-62-1398-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2b85/6064781/d63ac87048eb/FNR-62-1398-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2b85/6064781/3827a943a69f/FNR-62-1398-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2b85/6064781/5d1773aefe18/FNR-62-1398-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2b85/6064781/2511a7465ac8/FNR-62-1398-g003.jpg

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