Ferulic acid alleviates lipotoxicity-induced hepatocellular death through the SIRT1-regulated autophagy pathway and independently of AMPK and Akt in AML-12 hepatocytes.

Autophagy Ferulic acid Lipotoxicity Metabolic diseases SIRT1

Journal

Nutrition & metabolism
ISSN: 1743-7075
Titre abrégé: Nutr Metab (Lond)
Pays: England
ID NLM: 101231644

Informations de publication

Date de publication:
19 Jan 2021
Historique:
received: 22 10 2020
accepted: 02 01 2021
entrez: 20 1 2021
pubmed: 21 1 2021
medline: 21 1 2021
Statut: epublish

Résumé

Lipotoxicity-induced cell death plays a detrimental role in the pathogenesis of metabolic diseases. Ferulic acid, widespread in plant-based food, is a radical scavenger with multiple bioactivities. However, the benefits of ferulic acid against hepatic lipotoxicity are largely unclear. Here, we investigated the protective effect of ferulic acid against palmitate-induced lipotoxicity and clarified its potential mechanisms in AML-12 hepatocytes. AML-12 mouse hepatocytes were exposed to palmitate to mimic lipotoxicity. Different doses (25, 50, and 100 μM) of ferulic acid were added 2 h before palmitate treatment. Cell viability was detected by measuring lactate dehydrogenase release, nuclear staining, and the expression of cleaved-caspase-3. Intracellular reactive oxygen species content and mitochondrial membrane potential were analysed by fluorescent probes. The potential mechanisms were explored by molecular biological methods, including Western blotting and quantitative real-time PCR, and were further verified by siRNA interference. Our data showed that ferulic acid significantly inhibited palmitate-induced cell death, rescued mitochondrial membrane potential, reduced reactive oxygen species accumulation, and decreased inflammatory factor activation, including IL-6 and IL-1beta. Ferulic acid significantly stimulated autophagy in hepatocytes, whereas autophagy suppression blocked the protective effect of ferulic acid against lipotoxicity. Ferulic acid-activated autophagy, which was triggered by SIRT1 upregulation, was mechanistically involved in its anti-lipotoxicity effects. SIRT1 silencing blocked most beneficial changes induced by ferulic acid. We demonstrated that the phytochemical ferulic acid, which is found in plant-based food, protected against hepatic lipotoxicity, through the SIRT1/autophagy pathway. Increased intake of ferulic acid-enriched food is a potential strategy to prevent and/or improve metabolic diseases with lipotoxicity as a typical pathological feature.

Sections du résumé

BACKGROUND BACKGROUND
Lipotoxicity-induced cell death plays a detrimental role in the pathogenesis of metabolic diseases. Ferulic acid, widespread in plant-based food, is a radical scavenger with multiple bioactivities. However, the benefits of ferulic acid against hepatic lipotoxicity are largely unclear. Here, we investigated the protective effect of ferulic acid against palmitate-induced lipotoxicity and clarified its potential mechanisms in AML-12 hepatocytes.
METHODS METHODS
AML-12 mouse hepatocytes were exposed to palmitate to mimic lipotoxicity. Different doses (25, 50, and 100 μM) of ferulic acid were added 2 h before palmitate treatment. Cell viability was detected by measuring lactate dehydrogenase release, nuclear staining, and the expression of cleaved-caspase-3. Intracellular reactive oxygen species content and mitochondrial membrane potential were analysed by fluorescent probes. The potential mechanisms were explored by molecular biological methods, including Western blotting and quantitative real-time PCR, and were further verified by siRNA interference.
RESULTS RESULTS
Our data showed that ferulic acid significantly inhibited palmitate-induced cell death, rescued mitochondrial membrane potential, reduced reactive oxygen species accumulation, and decreased inflammatory factor activation, including IL-6 and IL-1beta. Ferulic acid significantly stimulated autophagy in hepatocytes, whereas autophagy suppression blocked the protective effect of ferulic acid against lipotoxicity. Ferulic acid-activated autophagy, which was triggered by SIRT1 upregulation, was mechanistically involved in its anti-lipotoxicity effects. SIRT1 silencing blocked most beneficial changes induced by ferulic acid.
CONCLUSIONS CONCLUSIONS
We demonstrated that the phytochemical ferulic acid, which is found in plant-based food, protected against hepatic lipotoxicity, through the SIRT1/autophagy pathway. Increased intake of ferulic acid-enriched food is a potential strategy to prevent and/or improve metabolic diseases with lipotoxicity as a typical pathological feature.

Identifiants

pubmed: 33468182
doi: 10.1186/s12986-021-00540-9
pii: 10.1186/s12986-021-00540-9
pmc: PMC7814733
doi:

Types de publication

Journal Article

Langues

eng

Pagination

13

Subventions

Organisme : Natural Science Foundation of China
ID : 81973041
Organisme : Natural Science Foundation of China
ID : 81773981
Organisme : Zhejiang Natural Science Foundation for Distinguished Young Scholars
ID : LR20H260001
Organisme : Research Fund of Zhejiang Chinese Medical University
ID : 771200F027

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Auteurs

Tiantian Xu (T)

College of Basic Medicine and Public Health, Zhejiang Chinese Medical University, Hangzhou, 310053, China.
College of Life Science, Zhejiang Chinese Medical University, Hangzhou, 310053, China.

Qing Song (Q)

College of Basic Medicine and Public Health, Zhejiang Chinese Medical University, Hangzhou, 310053, China.
College of Life Science, Zhejiang Chinese Medical University, Hangzhou, 310053, China.
Molecular Medicine Institute, Zhejiang Chinese Medical University, Hangzhou, 310053, China.

Li Zhou (L)

College of Life Science, Zhejiang Chinese Medical University, Hangzhou, 310053, China.
The First Affiliated Hospital of Zhejiang Chinese Medical University, Zhejiang Chinese Medical University, Hangzhou, 310053, China.

Wenwen Yang (W)

College of Basic Medicine and Public Health, Zhejiang Chinese Medical University, Hangzhou, 310053, China.
College of Life Science, Zhejiang Chinese Medical University, Hangzhou, 310053, China.

Xiangyao Wu (X)

College of Basic Medicine and Public Health, Zhejiang Chinese Medical University, Hangzhou, 310053, China.
College of Life Science, Zhejiang Chinese Medical University, Hangzhou, 310053, China.

Qianyu Qian (Q)

College of Life Science, Zhejiang Chinese Medical University, Hangzhou, 310053, China.
Molecular Medicine Institute, Zhejiang Chinese Medical University, Hangzhou, 310053, China.

Hui Chai (H)

College of Life Science, Zhejiang Chinese Medical University, Hangzhou, 310053, China.
Molecular Medicine Institute, Zhejiang Chinese Medical University, Hangzhou, 310053, China.

Qiang Han (Q)

College of Basic Medicine and Public Health, Zhejiang Chinese Medical University, Hangzhou, 310053, China.

Hongzhi Pan (H)

Collaborative Research Center, Shanghai University of Medicine and Health Sciences, Shanghai, 201399, China.

Xiaobing Dou (X)

College of Life Science, Zhejiang Chinese Medical University, Hangzhou, 310053, China. xbdou77@163.com.
Molecular Medicine Institute, Zhejiang Chinese Medical University, Hangzhou, 310053, China. xbdou77@163.com.

Songtao Li (S)

College of Basic Medicine and Public Health, Zhejiang Chinese Medical University, Hangzhou, 310053, China. lisongtao@vip.126.com.
Molecular Medicine Institute, Zhejiang Chinese Medical University, Hangzhou, 310053, China. lisongtao@vip.126.com.

Classifications MeSH