Rosmarinic acid alleviates ethanol-induced lipid accumulation by repressing fatty acid biosynthesis

Recent studies have demonstrated that rosmarinic acid is a valuable natural product for treatment of alcoholic liver disease. However, the mechanisms whereby rosmarinic acid improves alcoholic liver disease remain unclear. Here we performed experiments using a non-transformed mouse hepatocyte cell l...

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Published inFood & function Vol. 11; no. 3; pp. 294 - 216
Main Authors Guo, Chang, Shangguan, Yu, Zhang, Meiru, Ruan, Yanxin, Xue, Guoqing, Ma, Jingfan, Yang, Jian, Qiu, Longxin
Format Journal Article
LanguageEnglish
Published England Royal Society of Chemistry 01.03.2020
Subjects
Accumulation
Animals
Biomarkers
Biosynthesis
Carnitine
Cell Line
Cinnamates - pharmacology
Cytoplasm
Depsides - pharmacology
Ethanol
Ethanol - pharmacology
Fatty acids
Fatty Acids - biosynthesis
Fatty-acid synthase
Gene expression
Glycine
Hepatocytes - drug effects
Hepatocytes - metabolism
Interleukin 6
Lipid Metabolism
Lipids
Liver
Liver diseases
Malondialdehyde
Medical treatment
Metabolism
Metabolites
Metabolomics
Mice
Mitochondria
Natural products
Palmitic acid
Rosmarinic Acid
Sorbitol
Sterol regulatory element-binding protein
Stress, Physiological
Succinic acid
Tumor necrosis factor-α
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Abstract Recent studies have demonstrated that rosmarinic acid is a valuable natural product for treatment of alcoholic liver disease. However, the mechanisms whereby rosmarinic acid improves alcoholic liver disease remain unclear. Here we performed experiments using a non-transformed mouse hepatocyte cell line (AML12). Oil-red O staining demonstrated that rosmarinic acid reduced ethanol-induced lipid accumulation. It was shown that rosmarinic acid prevented ethanol-induced elevation of the malondialdehyde level. We also found that rosmarinic acid inhibited ethanol-induced mRNA expression of tumor necrosis factor-α and interleukin 6. Metabolomics analysis revealed that rosmarinic acid ameliorated ethanol-induced fatty acid biosynthesis in the cytoplasm. In addition, palmitic acid was a candidate biomarker in cells exposed to ethanol or ethanol plus rosmarinic acid. Rosmarinic acid prevented the ethanol-induced increase in sorbitol that is a component of the polyol pathway. Moreover, we confirmed that rosmarinic acid attenuated ethanol-induced mRNA expression of fatty acid synthase, probably by modulating the AMPK/SREBP-1c pathway. Furthermore, rosmarinic acid prevented the ethanol-induced decrease in eight metabolites that are involved in mitochondrial metabolism, including glycine and succinic acid which are the components of carnitine synthesis. These results provide a crucial insight into the molecular mechanism of rosmarinic acid in alleviating ethanol-induced injury. Rosmarinic acid ameliorates ethanol-induced lipid accumulation by reducing fatty acid biosynthesis and tumor necrosis factor-α.
AbstractList Recent studies have demonstrated that rosmarinic acid is a valuable natural product for treatment of alcoholic liver disease. However, the mechanisms whereby rosmarinic acid improves alcoholic liver disease remain unclear. Here we performed experiments using a non-transformed mouse hepatocyte cell line (AML12). Oil-red O staining demonstrated that rosmarinic acid reduced ethanol-induced lipid accumulation. It was shown that rosmarinic acid prevented ethanol-induced elevation of the malondialdehyde level. We also found that rosmarinic acid inhibited ethanol-induced mRNA expression of tumor necrosis factor-α and interleukin 6. Metabolomics analysis revealed that rosmarinic acid ameliorated ethanol-induced fatty acid biosynthesis in the cytoplasm. In addition, palmitic acid was a candidate biomarker in cells exposed to ethanol or ethanol plus rosmarinic acid. Rosmarinic acid prevented the ethanol-induced increase in sorbitol that is a component of the polyol pathway. Moreover, we confirmed that rosmarinic acid attenuated ethanol-induced mRNA expression of fatty acid synthase, probably by modulating the AMPK/SREBP-1c pathway. Furthermore, rosmarinic acid prevented the ethanol-induced decrease in eight metabolites that are involved in mitochondrial metabolism, including glycine and succinic acid which are the components of carnitine synthesis. These results provide a crucial insight into the molecular mechanism of rosmarinic acid in alleviating ethanol-induced injury.
Recent studies have demonstrated that rosmarinic acid is a valuable natural product for treatment of alcoholic liver disease. However, the mechanisms whereby rosmarinic acid improves alcoholic liver disease remain unclear. Here we performed experiments using a non-transformed mouse hepatocyte cell line (AML12). Oil-red O staining demonstrated that rosmarinic acid reduced ethanol-induced lipid accumulation. It was shown that rosmarinic acid prevented ethanol-induced elevation of the malondialdehyde level. We also found that rosmarinic acid inhibited ethanol-induced mRNA expression of tumor necrosis factor-α and interleukin 6. Metabolomics analysis revealed that rosmarinic acid ameliorated ethanol-induced fatty acid biosynthesis in the cytoplasm. In addition, palmitic acid was a candidate biomarker in cells exposed to ethanol or ethanol plus rosmarinic acid. Rosmarinic acid prevented the ethanol-induced increase in sorbitol that is a component of the polyol pathway. Moreover, we confirmed that rosmarinic acid attenuated ethanol-induced mRNA expression of fatty acid synthase, probably by modulating the AMPK/SREBP-1c pathway. Furthermore, rosmarinic acid prevented the ethanol-induced decrease in eight metabolites that are involved in mitochondrial metabolism, including glycine and succinic acid which are the components of carnitine synthesis. These results provide a crucial insight into the molecular mechanism of rosmarinic acid in alleviating ethanol-induced injury. Rosmarinic acid ameliorates ethanol-induced lipid accumulation by reducing fatty acid biosynthesis and tumor necrosis factor-α.
Author Shangguan, Yu
Guo, Chang
Yang, Jian
Ruan, Yanxin
Xue, Guoqing
Ma, Jingfan
Qiu, Longxin
Zhang, Meiru
AuthorAffiliation Key Laboratory of Preventive Veterinary Medicine and Biotechnology (Longyan University)
Fujian Provincial Key Laboratory for the Prevention and Control of Animal Infectious Diseases and Biotechnology
Fujian Province University
School of Life Sciences
Longyan University
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Snippet Recent studies have demonstrated that rosmarinic acid is a valuable natural product for treatment of alcoholic liver disease. However, the mechanisms whereby...
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StartPage 294
SubjectTerms Accumulation
Animals
Biomarkers
Biosynthesis
Carnitine
Cell Line
Cinnamates - pharmacology
Cytoplasm
Depsides - pharmacology
Ethanol
Ethanol - pharmacology
Fatty acids
Fatty Acids - biosynthesis
Fatty-acid synthase
Gene expression
Glycine
Hepatocytes - drug effects
Hepatocytes - metabolism
Interleukin 6
Lipid Metabolism
Lipids
Liver
Liver diseases
Malondialdehyde
Medical treatment
Metabolism
Metabolites
Metabolomics
Mice
Mitochondria
Natural products
Palmitic acid
Rosmarinic Acid
Sorbitol
Sterol regulatory element-binding protein
Stress, Physiological
Succinic acid
Tumor necrosis factor-α
Title Rosmarinic acid alleviates ethanol-induced lipid accumulation by repressing fatty acid biosynthesis
URI https://www.ncbi.nlm.nih.gov/pubmed/32129352
https://www.proquest.com/docview/2383023491
https://search.proquest.com/docview/2371144072
Volume 11
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