Garcinol Attenuates Lipoprotein(a)-Induced Oxidative Stress and Inflammatory Cytokine Production in Ventricular Cardiomyocyte through α7-Nicotinic Acetylcholine Receptor-Mediated Inhibition of the p38 MAPK and NF-κB Signaling Pathways.

Nen-Chung Chang; Chi-Tai Yeh; Yen-Kuang Lin; Kuang-Tai Kuo; Iat-Hang Fong; Iat-Hang Fong; Nicholas G Kounis; Patrick Hu; Ming-Yow Hung

doi:10.3390/ANTIOX10030461

Garcinol Attenuates Lipoprotein(a)-Induced Oxidative Stress and Inflammatory Cytokine Production in Ventricular Cardiomyocyte through α7-Nicotinic Acetylcholine Receptor-Mediated Inhibition of the p38 MAPK and NF-κB Signaling Pathways.

Nen-Chung Chang
, Chi-Tai Yeh
, Yen-Kuang Lin
, Kuang-Tai Kuo
, Iat-Hang Fong
, Iat-Hang Fong
, Nicholas G Kounis
, Patrick Hu
, Ming-Yow Hung

Taipei Medical University Hospital
Taipei Medical University
Yuanpei University
University of Patras
University of California, Riverside

Research output: Contribution to journal › Article › peer-review

Original language	American English
Journal	Antioxidants
Volume	10
Issue number	3
DOIs	https://doi.org/10.3390/ANTIOX10030461
State	Published - Mar 16 2021
Externally published	Yes

Disciplines

Pharmacology

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10.3390/ANTIOX10030461License: Unspecified

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Chang, N.-C., Yeh, C.-T., Lin, Y.-K., Kuo, K.-T., Fong, I.-H., Fong, I.-H., Kounis, N. G., Hu, P., & Hung, M.-Y. (2021). Garcinol Attenuates Lipoprotein(a)-Induced Oxidative Stress and Inflammatory Cytokine Production in Ventricular Cardiomyocyte through α7-Nicotinic Acetylcholine Receptor-Mediated Inhibition of the p38 MAPK and NF-κB Signaling Pathways. Antioxidants, 10(3). https://doi.org/10.3390/ANTIOX10030461

Garcinol Attenuates Lipoprotein(a)-Induced Oxidative Stress and Inflammatory Cytokine Production in Ventricular Cardiomyocyte through α7-Nicotinic Acetylcholine Receptor-Mediated Inhibition of the p38 MAPK and NF-κB Signaling Pathways. / Chang, Nen-Chung; Yeh, Chi-Tai; Lin, Yen-Kuang et al.
In: Antioxidants, Vol. 10, No. 3, 16.03.2021.

Research output: Contribution to journal › Article › peer-review

Chang, N-C, Yeh, C-T, Lin, Y-K, Kuo, K-T, Fong, I-H, Fong, I-H, Kounis, NG, Hu, P & Hung, M-Y 2021, 'Garcinol Attenuates Lipoprotein(a)-Induced Oxidative Stress and Inflammatory Cytokine Production in Ventricular Cardiomyocyte through α7-Nicotinic Acetylcholine Receptor-Mediated Inhibition of the p38 MAPK and NF-κB Signaling Pathways.', Antioxidants, vol. 10, no. 3. https://doi.org/10.3390/ANTIOX10030461

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title = "Garcinol Attenuates Lipoprotein(a)-Induced Oxidative Stress and Inflammatory Cytokine Production in Ventricular Cardiomyocyte through α7-Nicotinic Acetylcholine Receptor-Mediated Inhibition of the p38 MAPK and NF-κB Signaling Pathways.",

author = "Nen-Chung Chang and Chi-Tai Yeh and Yen-Kuang Lin and Kuang-Tai Kuo and Iat-Hang Fong and Iat-Hang Fong and Kounis, \{Nicholas G\} and Patrick Hu and Ming-Yow Hung",

note = "Nazha Hamdani, Academic Editor Garcinol, a nicotinic acetylcholine receptor (nAChR) antagonist, has recently been established as an anti-inflammation agent. However, the molecular mechanism by which garcinol suppresses inflammation in the context of acute myocardial infarction (AMI) remains unclear.",

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AU - Chang, Nen-Chung

AU - Yeh, Chi-Tai

AU - Lin, Yen-Kuang

AU - Kuo, Kuang-Tai

AU - Fong, Iat-Hang

AU - Kounis, Nicholas G

AU - Hu, Patrick

AU - Hung, Ming-Yow

N1 - Nazha Hamdani, Academic Editor Garcinol, a nicotinic acetylcholine receptor (nAChR) antagonist, has recently been established as an anti-inflammation agent. However, the molecular mechanism by which garcinol suppresses inflammation in the context of acute myocardial infarction (AMI) remains unclear.

PY - 2021/3/16

Y1 - 2021/3/16

UR - https://europepmc.org/article/MED/33809417

U2 - 10.3390/ANTIOX10030461

DO - 10.3390/ANTIOX10030461

M3 - Article

VL - 10

JO - Antioxidants

JF - Antioxidants

IS - 3

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Garcinol Attenuates Lipoprotein(a)-Induced Oxidative Stress and Inflammatory Cytokine Production in Ventricular Cardiomyocyte through α7-Nicotinic Acetylcholine Receptor-Mediated Inhibition of the p38 MAPK and NF-κB Signaling Pathways.

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