Syringaldehyde Alleviates Cardiac Hypertrophy Induced by Hyperglycemia in H9c2 Cells Through GLP-1 Receptor Signals

Background: Cardiac hypertrophy is a significant complication of diabetes, often triggered by hyperglycemia. Glucagon-like peptide-1 (GLP-1) receptor agonists alleviate cardiac hypertrophy, but their efficacy diminishes under GLP-1 resistance. Syringaldehyde (SA), a natural phenolic compound, may ac...

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Published inPharmaceuticals (Basel, Switzerland) Vol. 18; no. 1; p. 110
Main Authors Li, Yingxiao, Hsu, Chao-Tien, Yang, Ting-Ting, Cheng, Kai-Chun
Format Journal Article
LanguageEnglish
Published Switzerland MDPI AG 01.01.2025
MDPI
Subjects
Aldehydes
AMPK
Biomarkers
cardiac hypertrophy
Cardiomyocytes
Cardiomyopathy
Care and treatment
Cellular signal transduction
Complications and side effects
Diabetes
diabetes complications
Diabetic angiopathies
GLP-1 receptor agonists
GLP-1 resistance
Glucose
Health aspects
Heart attacks
Heart enlargement
Heart failure
Hyperglycemia
Kinases
O-linked N-acetylglucosamine transferase (OGT)
Oxidative stress
Peptides
Physiology
Proteins
syringaldehyde
Testing
Taiwan
AMPK
O-linked N-acetylglucosamine transferase (OGT)
syringaldehyde
diabetes complications
cardiac hypertrophy
GLP-1 resistance
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Abstract Background: Cardiac hypertrophy is a significant complication of diabetes, often triggered by hyperglycemia. Glucagon-like peptide-1 (GLP-1) receptor agonists alleviate cardiac hypertrophy, but their efficacy diminishes under GLP-1 resistance. Syringaldehyde (SA), a natural phenolic compound, may activate GLP-1 receptors and mitigate hypertrophy. This study explores SA’s therapeutic potential in hyperglycemia-induced cardiac hypertrophy in H9c2 cardiomyocytes. Methods: H9c2 cells were exposed to high glucose to induce hypertrophy. Cells were treated with varying SA concentrations, and hypertrophic biomarkers were analyzed using ELISA, qPCR, and Western blot. Results: SA reduced cell size and hypertrophic biomarkers in a dose-dependent manner while increasing GLP-1 receptor expression and cAMP levels. These effects were attenuated in GLP-1-resistant cells, highlighting the role of GLP-1 receptor activation. AMPK activation was essential, as its inhibition abolished SA’s effects. SA also decreased O-linked N-acetylglucosamine transferase (OGT) expression via AMPK activation, contributing to reduced hypertrophy. Conclusions: SA alleviates hyperglycemia-induced cardiac hypertrophy in H9c2 cells by activating the GLP-1 receptor and AMPK signaling pathway.
AbstractList Background: Cardiac hypertrophy is a significant complication of diabetes, often triggered by hyperglycemia. Glucagon-like peptide-1 (GLP-1) receptor agonists alleviate cardiac hypertrophy, but their efficacy diminishes under GLP-1 resistance. Syringaldehyde (SA), a natural phenolic compound, may activate GLP-1 receptors and mitigate hypertrophy. This study explores SA’s therapeutic potential in hyperglycemia-induced cardiac hypertrophy in H9c2 cardiomyocytes. Methods: H9c2 cells were exposed to high glucose to induce hypertrophy. Cells were treated with varying SA concentrations, and hypertrophic biomarkers were analyzed using ELISA, qPCR, and Western blot. Results: SA reduced cell size and hypertrophic biomarkers in a dose-dependent manner while increasing GLP-1 receptor expression and cAMP levels. These effects were attenuated in GLP-1-resistant cells, highlighting the role of GLP-1 receptor activation. AMPK activation was essential, as its inhibition abolished SA’s effects. SA also decreased O-linked N-acetylglucosamine transferase (OGT) expression via AMPK activation, contributing to reduced hypertrophy. Conclusions: SA alleviates hyperglycemia-induced cardiac hypertrophy in H9c2 cells by activating the GLP-1 receptor and AMPK signaling pathway.
Background: Cardiac hypertrophy is a significant complication of diabetes, often triggered by hyperglycemia. Glucagon-like peptide-1 (GLP-1) receptor agonists alleviate cardiac hypertrophy, but their efficacy diminishes under GLP-1 resistance. Syringaldehyde (SA), a natural phenolic compound, may activate GLP-1 receptors and mitigate hypertrophy. This study explores SA’s therapeutic potential in hyperglycemia-induced cardiac hypertrophy in H9c2 cardiomyocytes. Methods: H9c2 cells were exposed to high glucose to induce hypertrophy. Cells were treated with varying SA concentrations, and hypertrophic biomarkers were analyzed using ELISA, qPCR, and Western blot. Results: SA reduced cell size and hypertrophic biomarkers in a dose-dependent manner while increasing GLP-1 receptor expression and cAMP levels. These effects were attenuated in GLP-1-resistant cells, highlighting the role of GLP-1 receptor activation. AMPK activation was essential, as its inhibition abolished SA’s effects. SA also decreased O-linked N-acetylglucosamine transferase (OGT) expression via AMPK activation, contributing to reduced hypertrophy. Conclusions: SA alleviates hyperglycemia-induced cardiac hypertrophy in H9c2 cells by activating the GLP-1 receptor and AMPK signaling pathway.
Cardiac hypertrophy is a significant complication of diabetes, often triggered by hyperglycemia. Glucagon-like peptide-1 (GLP-1) receptor agonists alleviate cardiac hypertrophy, but their efficacy diminishes under GLP-1 resistance. Syringaldehyde (SA), a natural phenolic compound, may activate GLP-1 receptors and mitigate hypertrophy. This study explores SA's therapeutic potential in hyperglycemia-induced cardiac hypertrophy in H9c2 cardiomyocytes. H9c2 cells were exposed to high glucose to induce hypertrophy. Cells were treated with varying SA concentrations, and hypertrophic biomarkers were analyzed using ELISA, qPCR, and Western blot. SA reduced cell size and hypertrophic biomarkers in a dose-dependent manner while increasing GLP-1 receptor expression and cAMP levels. These effects were attenuated in GLP-1-resistant cells, highlighting the role of GLP-1 receptor activation. AMPK activation was essential, as its inhibition abolished SA's effects. SA also decreased O-linked N-acetylglucosamine transferase (OGT) expression via AMPK activation, contributing to reduced hypertrophy. SA alleviates hyperglycemia-induced cardiac hypertrophy in H9c2 cells by activating the GLP-1 receptor and AMPK signaling pathway.
Background: Cardiac hypertrophy is a significant complication of diabetes, often triggered by hyperglycemia. Glucagon-like peptide-1 (GLP-1) receptor agonists alleviate cardiac hypertrophy, but their efficacy diminishes under GLP-1 resistance. Syringaldehyde (SA), a natural phenolic compound, may activate GLP-1 receptors and mitigate hypertrophy. This study explores SA's therapeutic potential in hyperglycemia-induced cardiac hypertrophy in H9c2 cardiomyocytes. Methods: H9c2 cells were exposed to high glucose to induce hypertrophy. Cells were treated with varying SA concentrations, and hypertrophic biomarkers were analyzed using ELISA, qPCR, and Western blot. Results: SA reduced cell size and hypertrophic biomarkers in a dose-dependent manner while increasing GLP-1 receptor expression and cAMP levels. These effects were attenuated in GLP-1-resistant cells, highlighting the role of GLP-1 receptor activation. AMPK activation was essential, as its inhibition abolished SA's effects. SA also decreased O-linked N-acetylglucosamine transferase (OGT) expression via AMPK activation, contributing to reduced hypertrophy. Conclusions: SA alleviates hyperglycemia-induced cardiac hypertrophy in H9c2 cells by activating the GLP-1 receptor and AMPK signaling pathway.Background: Cardiac hypertrophy is a significant complication of diabetes, often triggered by hyperglycemia. Glucagon-like peptide-1 (GLP-1) receptor agonists alleviate cardiac hypertrophy, but their efficacy diminishes under GLP-1 resistance. Syringaldehyde (SA), a natural phenolic compound, may activate GLP-1 receptors and mitigate hypertrophy. This study explores SA's therapeutic potential in hyperglycemia-induced cardiac hypertrophy in H9c2 cardiomyocytes. Methods: H9c2 cells were exposed to high glucose to induce hypertrophy. Cells were treated with varying SA concentrations, and hypertrophic biomarkers were analyzed using ELISA, qPCR, and Western blot. Results: SA reduced cell size and hypertrophic biomarkers in a dose-dependent manner while increasing GLP-1 receptor expression and cAMP levels. These effects were attenuated in GLP-1-resistant cells, highlighting the role of GLP-1 receptor activation. AMPK activation was essential, as its inhibition abolished SA's effects. SA also decreased O-linked N-acetylglucosamine transferase (OGT) expression via AMPK activation, contributing to reduced hypertrophy. Conclusions: SA alleviates hyperglycemia-induced cardiac hypertrophy in H9c2 cells by activating the GLP-1 receptor and AMPK signaling pathway.
Audience Academic
Author Li, Yingxiao
Yang, Ting-Ting
Hsu, Chao-Tien
Cheng, Kai-Chun
AuthorAffiliation 1 Department of Anatomy, College of Medicine, I-Shou University, Kaohsiung 824005, Taiwan; yxli0809@isu.edu.tw
4 Department of Pharmacy, College of Pharmacy and Health Care, Tajen University, Pingtung 90741, Taiwan
3 School of Chinese Medicine for Post Baccalaureate, College of Medicine, I-Shou University, Kaohsiung 824005, Taiwan; tingting@isu.edu.tw
2 Department of Pathology, E-Da Hospital, I-Shou University, Kaohsiung 824005, Taiwan; ed103797@edah.org.tw
AuthorAffiliation_xml – name: 1 Department of Anatomy, College of Medicine, I-Shou University, Kaohsiung 824005, Taiwan; yxli0809@isu.edu.tw
– name: 2 Department of Pathology, E-Da Hospital, I-Shou University, Kaohsiung 824005, Taiwan; ed103797@edah.org.tw
– name: 3 School of Chinese Medicine for Post Baccalaureate, College of Medicine, I-Shou University, Kaohsiung 824005, Taiwan; tingting@isu.edu.tw
– name: 4 Department of Pharmacy, College of Pharmacy and Health Care, Tajen University, Pingtung 90741, Taiwan
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  surname: Li
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  givenname: Chao-Tien
  surname: Hsu
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  surname: Yang
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  givenname: Kai-Chun
  surname: Cheng
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BackLink https://www.ncbi.nlm.nih.gov/pubmed/39861172$$D View this record in MEDLINE/PubMed
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Keywords AMPK
O-linked N-acetylglucosamine transferase (OGT)
syringaldehyde
diabetes complications
cardiac hypertrophy
GLP-1 resistance
Language English
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Snippet Background: Cardiac hypertrophy is a significant complication of diabetes, often triggered by hyperglycemia. Glucagon-like peptide-1 (GLP-1) receptor agonists...
Cardiac hypertrophy is a significant complication of diabetes, often triggered by hyperglycemia. Glucagon-like peptide-1 (GLP-1) receptor agonists alleviate...
Background: Cardiac hypertrophy is a significant complication of diabetes, often triggered by hyperglycemia. Glucagon-like peptide-1 (GLP-1) receptor agonists...
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StartPage 110
SubjectTerms Aldehydes
AMPK
Biomarkers
cardiac hypertrophy
Cardiomyocytes
Cardiomyopathy
Care and treatment
Cellular signal transduction
Complications and side effects
Diabetes
diabetes complications
Diabetic angiopathies
GLP-1 receptor agonists
GLP-1 resistance
Glucose
Health aspects
Heart attacks
Heart enlargement
Heart failure
Hyperglycemia
Kinases
O-linked N-acetylglucosamine transferase (OGT)
Oxidative stress
Peptides
Physiology
Proteins
syringaldehyde
Testing
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Title Syringaldehyde Alleviates Cardiac Hypertrophy Induced by Hyperglycemia in H9c2 Cells Through GLP-1 Receptor Signals
URI https://www.ncbi.nlm.nih.gov/pubmed/39861172
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https://pubmed.ncbi.nlm.nih.gov/PMC11768131
https://doaj.org/article/67c004b2fb144c0bae436059bd8ff7e5
Volume 18
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