ReferenceID 2405
Methyl Brevifolincarboxylate Attenuates Free Fatty Acid-Induced Lipid Metabolism and Inflammation in Hepatocytes through AMPK/NF-κB Signaling Pathway
Int J Mol Sci
The prevalence of non-alcoholic fatty liver disease (NAFLD) is one of the leading causes of chronic liver diseases worldwide. This study examined the potential protective effects of a naturally occurring polyphenolic com
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- Reference Id
- 2405
- Evidence Id
- 18995
- Core Evidence Id
- 18995
- Source Reference Id
- 4834
- Herb2 Reference Id
- HBREF005631
- Subject Paper Key
- HBIN035118_34576229
- Pubmed Id
- 34576229
- Doi
- 10.3390/ijms221810062
- Paper Title
- Methyl Brevifolincarboxylate Attenuates Free Fatty Acid-Induced Lipid Metabolism and Inflammation in Hepatocytes through AMPK/NF-κB Signaling Pathway
- Paper Abstract
- The prevalence of non-alcoholic fatty liver disease (NAFLD) is one of the leading causes of chronic liver diseases worldwide. This study examined the potential protective effects of a naturally occurring polyphenolic compound, methyl brevifolincarboxylate (MBC) on fatty liver injury in vitro. The results showed that MBC at its non-cytotoxic concentrations, reduced lipid droplet accumulation and triglyceride (TG) levels in the oleic acid (OA)-treated human hepatocarcinoma cell line, SK-HEP-1 and murine primary hepatocytes. In OA-treated SK-HEP-1 cells and primary murine hepatocytes, MBC attenuated the mRNA expression levels of the de novo lipogenesis molecules, acetyl-coenzyme A carboxylase (Acc1), fatty acid synthase (Fasn) and sterol regulatory element binding protein 1c (Srebp1c). MBC promoted the lipid oxidation factor peroxisome proliferator activated receptor-alpha (Pparalpha), and its target genes, carnitine palmitoyl transferase 1 (Cpt1) and acyl-coenzyme A oxidase 1 (Acox1) in both the SK-HEP-1 cells and primary murine hepatocytes. The mRNA results were further supported by the attenuated protein expression of lipogenesis and lipid oxidation molecules in OA-treated SK-HEP-1 cells. The MBC increased the expression of AMP activated protein kinase (AMPK) phosphorylation. On the other hand, MBC treatment dampened the inflammatory mediator's, tumor necrosis factor (TNF)-alpha, interleukin-6 (IL-6), IL-8, and IL-1beta secretion, and nuclear factor (NF)-kappaB expression (mRNA and protein) through reduced reactive oxygen species production in OA-treated SK-HEP-1 cells. Taken together, our results demonstrated that MBC possessed potential protective effects against NAFLD in vitro by amelioration of lipid metabolism and inflammatory markers through the AMPK/NF-kappaB signaling pathway.
- Journal
- Int J Mol Sci
- Publish Year
- 2021
- Experiment Subject
- mouse; human; human hepatocarcinoma cell line; oa-treated sk-hep-1 cells; sk-hep-1 cells
- Experiment Type
- Cell Experiment
- Phenotype Related
- Hepatocarcinoma; Tumor; Non-alcoholic Fatty Liver Disease; Chronic Liver Diseases
- Paper Title Cn
- Paper Title En
- Methyl Brevifolincarboxylate Attenuates Free Fatty Acid-Induced Lipid Metabolism and Inflammation in Hepatocytes through AMPK/NF-κB Signaling Pathway
- Bilingual Status
- semi_complete