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反式茴香脑对肝细胞脂代谢的调节作用。

Modulation of Lipid Metabolism by Trans-Anethole in Hepatocytes.

机构信息

Department of Integrated Biomedical and Life Science, College of Health Science, Korea University, Seoul 02841, Korea.

Department of Clinical Laboratory Sciences, College of Health Science, Korea University, Seoul 02841, Korea.

出版信息

Molecules. 2020 Oct 26;25(21):4946. doi: 10.3390/molecules25214946.

DOI:10.3390/molecules25214946
PMID:33114589
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7662808/
Abstract

Non-alcoholic fatty liver disease is caused by excessive lipid accumulation in hepatocytes. Although trans-anethole (TAO) affects hypoglycemia and has anti-immune activity and anti-obesity effects, its role in non-alcoholic fatty liver disease remains unknown. This study aimed to evaluate the effects of TAO on cellular senescence, lipid metabolism, and reinforcement of microenvironments in HepG2 cells. To analyze the lipid metabolic activity of TAO, PCR analysis, flow-cytometry, and Oil Red O staining were performed, and mitochondrial membrane potential (MMP) and cellular senescence kits were used for assessing the suppression of cellular senescence. At 2000 μg/mL TAO, the cellular viability was approximately 99%, and cell senescence decreased dose-dependently. In the results for MMP, activity increased with concentration. The levels of lipolytic genes, , and , strongly increased over 3 days and the levels of lipogenic genes, and , were downregulated on the first day at 1000 μg/mL TAO. Consequently, it was found that TAO affects the suppression of cellular senescence, activation of lipid metabolism, and reinforcement of the microenvironment in HepG2 cells, and can be added as a useful component to functional foods to prevent fatty liver disease and cellular senescence, as well as increase the immunoactivity of the liver.

摘要

非酒精性脂肪性肝病是由肝细胞内脂质积聚过多引起的。尽管茴脑(TAO)会影响血糖水平,具有免疫活性和抗肥胖作用,但它在非酒精性脂肪性肝病中的作用尚不清楚。本研究旨在评估 TAO 对 HepG2 细胞细胞衰老、脂代谢和微环境强化的影响。为了分析 TAO 的脂代谢活性,进行了 PCR 分析、流式细胞术和油红 O 染色,并用线粒体膜电位(MMP)和细胞衰老试剂盒评估细胞衰老的抑制作用。在 2000μg/mL TAO 下,细胞活力约为 99%,细胞衰老呈剂量依赖性下降。在 MMP 的结果中,活性随浓度增加而增加。在 1000μg/mL TAO 下,脂解基因和的水平在 3 天内强烈增加,而脂生成基因和的水平在第一天就被下调。因此,发现 TAO 影响细胞衰老的抑制、脂代谢的激活和 HepG2 细胞微环境的强化,可作为功能性食品的有用成分添加,以预防脂肪肝疾病和细胞衰老,并提高肝脏的免疫活性。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b170/7662808/8042a6421ed5/molecules-25-04946-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b170/7662808/28b6d2ef572f/molecules-25-04946-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b170/7662808/26e5731632e2/molecules-25-04946-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b170/7662808/13c12225d93c/molecules-25-04946-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b170/7662808/487dfdf0a8ea/molecules-25-04946-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b170/7662808/d62aa1e465a6/molecules-25-04946-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b170/7662808/8042a6421ed5/molecules-25-04946-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b170/7662808/28b6d2ef572f/molecules-25-04946-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b170/7662808/26e5731632e2/molecules-25-04946-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b170/7662808/13c12225d93c/molecules-25-04946-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b170/7662808/487dfdf0a8ea/molecules-25-04946-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b170/7662808/d62aa1e465a6/molecules-25-04946-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b170/7662808/8042a6421ed5/molecules-25-04946-g006.jpg

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