Nobiletin ameliorates cardiac impairment and alleviates cardiac remodeling after acute myocardial infarction in rats via JNK regulation

Nobiletin was found to protect against acute myocardial infarction (AMI)‐induced cardiac function decline and myocardial remodeling, although the dose–effect relationship and underlying pathways remained unclear. In the current research, different doses of Nobiletin (7.5, 15 and 30 mg/kg/day) were a...

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Published inPharmacology research & perspectives Vol. 9; no. 2; pp. e00728 - n/a
Main Authors Liu, Zumei, Gao, Zhimin, Zeng, Lihuan, Liang, Zhenye, Zheng, Dechong, Wu, Xiaoqian
Format Journal Article
LanguageEnglish
Published United States John Wiley & Sons, Inc 01.04.2021
John Wiley and Sons Inc
Wiley
Subjects
acute myocardial infarction
Animals
Apoptosis
Apoptosis - drug effects
Autophagy
cardiac remodeling
Cardiotonic Agents - pharmacology
Cardiotonic Agents - therapeutic use
Cell Line
Coronary vessels
Disease Models, Animal
Dose-Response Relationship, Drug
Flavones - pharmacology
Flavones - therapeutic use
Gene expression
Glucose
Heart attacks
Humans
hypertrophy
Ischemia
JNK Mitogen-Activated Protein Kinases - antagonists & inhibitors
JNK Mitogen-Activated Protein Kinases - metabolism
Kinases
Laboratory animals
Male
MAP Kinase Signaling System - drug effects
Medical research
Myoblasts - drug effects
Myoblasts - pathology
Myocardial Infarction - complications
Myocardial Infarction - drug therapy
Myocardial Infarction - pathology
Myocardium - cytology
Myocardium - pathology
nobiletin
Original
Ostomy
Pharmacology
Phosphorylation
Proteins
Rats
Ventricular Remodeling - drug effects
apoptosis
nobiletin
hypertrophy
acute myocardial infarction
cardiac remodeling
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Abstract Nobiletin was found to protect against acute myocardial infarction (AMI)‐induced cardiac function decline and myocardial remodeling, although the dose–effect relationship and underlying pathways remained unclear. In the current research, different doses of Nobiletin (7.5, 15 and 30 mg/kg/day) were administered to AMI rat model for 21 days. Survival rate, echocardiography, and histological analysis were assessed in vivo. In addition, MTT assay, flow cytometry, and Western blotting were conducted to explore Nobiletin's cytotoxicity and antiapoptotic effect on H9C2 cells. Mechanistically, the activation of MAPK effectors and p38 in vivo was studied. The results showed medium‐ and high‐dose Nobiletin could significantly improve survival rate and cardiac function and reduce the area of infarction and cardiac fibrosis. Medium dose showed the best protection on cardiac functions, whereas high dose showed the best protective effect on cellular apoptosis and histological changes. JNK activation was significantly inhibited by Nobiletin in vivo, which could help to explain the partial contribution of autophagy to AMI‐induced apoptosis and the discrepancy on dose–effect relationships. Together, our study suggested that JNK inhibition plays an important role in Nobiletin‐induced antiapoptotic effect in myocardial infarction, and medium‐dose Nobiletin demonstrated the strongest effect in vivo.
AbstractList Abstract Nobiletin was found to protect against acute myocardial infarction (AMI)‐induced cardiac function decline and myocardial remodeling, although the dose–effect relationship and underlying pathways remained unclear. In the current research, different doses of Nobiletin (7.5, 15 and 30 mg/kg/day) were administered to AMI rat model for 21 days. Survival rate, echocardiography, and histological analysis were assessed in vivo. In addition, MTT assay, flow cytometry, and Western blotting were conducted to explore Nobiletin's cytotoxicity and antiapoptotic effect on H9C2 cells. Mechanistically, the activation of MAPK effectors and p38 in vivo was studied. The results showed medium‐ and high‐dose Nobiletin could significantly improve survival rate and cardiac function and reduce the area of infarction and cardiac fibrosis. Medium dose showed the best protection on cardiac functions, whereas high dose showed the best protective effect on cellular apoptosis and histological changes. JNK activation was significantly inhibited by Nobiletin in vivo, which could help to explain the partial contribution of autophagy to AMI‐induced apoptosis and the discrepancy on dose–effect relationships. Together, our study suggested that JNK inhibition plays an important role in Nobiletin‐induced antiapoptotic effect in myocardial infarction, and medium‐dose Nobiletin demonstrated the strongest effect in vivo.
Abstract Nobiletin was found to protect against acute myocardial infarction (AMI)‐induced cardiac function decline and myocardial remodeling, although the dose–effect relationship and underlying pathways remained unclear. In the current research, different doses of Nobiletin (7.5, 15 and 30 mg/kg/day) were administered to AMI rat model for 21 days. Survival rate, echocardiography, and histological analysis were assessed in vivo. In addition, MTT assay, flow cytometry, and Western blotting were conducted to explore Nobiletin's cytotoxicity and antiapoptotic effect on H9C2 cells. Mechanistically, the activation of MAPK effectors and p38 in vivo was studied. The results showed medium‐ and high‐dose Nobiletin could significantly improve survival rate and cardiac function and reduce the area of infarction and cardiac fibrosis. Medium dose showed the best protection on cardiac functions, whereas high dose showed the best protective effect on cellular apoptosis and histological changes. JNK activation was significantly inhibited by Nobiletin in vivo, which could help to explain the partial contribution of autophagy to AMI‐induced apoptosis and the discrepancy on dose–effect relationships. Together, our study suggested that JNK inhibition plays an important role in Nobiletin‐induced antiapoptotic effect in myocardial infarction, and medium‐dose Nobiletin demonstrated the strongest effect in vivo.
Nobiletin was found to protect against acute myocardial infarction (AMI)‐induced cardiac function decline and myocardial remodeling, although the dose–effect relationship and underlying pathways remained unclear. In the current research, different doses of Nobiletin (7.5, 15 and 30 mg/kg/day) were administered to AMI rat model for 21 days. Survival rate, echocardiography, and histological analysis were assessed in vivo. In addition, MTT assay, flow cytometry, and Western blotting were conducted to explore Nobiletin's cytotoxicity and antiapoptotic effect on H9C2 cells. Mechanistically, the activation of MAPK effectors and p38 in vivo was studied. The results showed medium‐ and high‐dose Nobiletin could significantly improve survival rate and cardiac function and reduce the area of infarction and cardiac fibrosis. Medium dose showed the best protection on cardiac functions, whereas high dose showed the best protective effect on cellular apoptosis and histological changes. JNK activation was significantly inhibited by Nobiletin in vivo, which could help to explain the partial contribution of autophagy to AMI‐induced apoptosis and the discrepancy on dose–effect relationships. Together, our study suggested that JNK inhibition plays an important role in Nobiletin‐induced antiapoptotic effect in myocardial infarction, and medium‐dose Nobiletin demonstrated the strongest effect in vivo.
Nobiletin was found to protect against acute myocardial infarction (AMI)-induced cardiac function decline and myocardial remodeling, although the dose-effect relationship and underlying pathways remained unclear. In the current research, different doses of Nobiletin (7.5, 15 and 30 mg/kg/day) were administered to AMI rat model for 21 days. Survival rate, echocardiography, and histological analysis were assessed in vivo. In addition, MTT assay, flow cytometry, and Western blotting were conducted to explore Nobiletin's cytotoxicity and antiapoptotic effect on H9C2 cells. Mechanistically, the activation of MAPK effectors and p38 in vivo was studied. The results showed medium- and high-dose Nobiletin could significantly improve survival rate and cardiac function and reduce the area of infarction and cardiac fibrosis. Medium dose showed the best protection on cardiac functions, whereas high dose showed the best protective effect on cellular apoptosis and histological changes. JNK activation was significantly inhibited by Nobiletin in vivo, which could help to explain the partial contribution of autophagy to AMI-induced apoptosis and the discrepancy on dose-effect relationships. Together, our study suggested that JNK inhibition plays an important role in Nobiletin-induced antiapoptotic effect in myocardial infarction, and medium-dose Nobiletin demonstrated the strongest effect in vivo.Nobiletin was found to protect against acute myocardial infarction (AMI)-induced cardiac function decline and myocardial remodeling, although the dose-effect relationship and underlying pathways remained unclear. In the current research, different doses of Nobiletin (7.5, 15 and 30 mg/kg/day) were administered to AMI rat model for 21 days. Survival rate, echocardiography, and histological analysis were assessed in vivo. In addition, MTT assay, flow cytometry, and Western blotting were conducted to explore Nobiletin's cytotoxicity and antiapoptotic effect on H9C2 cells. Mechanistically, the activation of MAPK effectors and p38 in vivo was studied. The results showed medium- and high-dose Nobiletin could significantly improve survival rate and cardiac function and reduce the area of infarction and cardiac fibrosis. Medium dose showed the best protection on cardiac functions, whereas high dose showed the best protective effect on cellular apoptosis and histological changes. JNK activation was significantly inhibited by Nobiletin in vivo, which could help to explain the partial contribution of autophagy to AMI-induced apoptosis and the discrepancy on dose-effect relationships. Together, our study suggested that JNK inhibition plays an important role in Nobiletin-induced antiapoptotic effect in myocardial infarction, and medium-dose Nobiletin demonstrated the strongest effect in vivo.
Nobiletin was found to protect against acute myocardial infarction (AMI)‐induced cardiac function decline and myocardial remodeling, although the dose–effect relationship and underlying pathways remained unclear. In the current research, different doses of Nobiletin (7.5, 15 and 30 mg/kg/day) were administered to AMI rat model for 21 days. Survival rate, echocardiography, and histological analysis were assessed in vivo. In addition, MTT assay, flow cytometry, and Western blotting were conducted to explore Nobiletin's cytotoxicity and antiapoptotic effect on H9C2 cells. Mechanistically, the activation of MAPK effectors and p38 in vivo was studied. The results showed medium‐ and high‐dose Nobiletin could significantly improve survival rate and cardiac function and reduce the area of infarction and cardiac fibrosis. Medium dose showed the best protection on cardiac functions, whereas high dose showed the best protective effect on cellular apoptosis and histological changes. JNK activation was significantly inhibited by Nobiletin in vivo, which could help to explain the partial contribution of autophagy to AMI‐induced apoptosis and the discrepancy on dose–effect relationships. Together, our study suggested that JNK inhibition plays an important role in Nobiletin‐induced antiapoptotic effect in myocardial infarction, and medium‐dose Nobiletin demonstrated the strongest effect in vivo.
Author Wu, Xiaoqian
Liu, Zumei
Zeng, Lihuan
Liang, Zhenye
Gao, Zhimin
Zheng, Dechong
AuthorAffiliation 2 Department of Central Laboratory Guangdong Second Provincial General Hospital Guangzhou Guangdong PR China
1 Key Laboratory of Molecular Target & Clinical Pharmacology and the State Key Laboratory of Respiratory Disease School of Pharmaceutical Sciences The Fifth Affiliated Hospital Guangzhou Medical University Guangzhou PR China
3 State Key Laboratory of Quality Research in Chinese Medicine Macau University of Science and Technology Macau PR China
AuthorAffiliation_xml – name: 3 State Key Laboratory of Quality Research in Chinese Medicine Macau University of Science and Technology Macau PR China
– name: 2 Department of Central Laboratory Guangdong Second Provincial General Hospital Guangzhou Guangdong PR China
– name: 1 Key Laboratory of Molecular Target & Clinical Pharmacology and the State Key Laboratory of Respiratory Disease School of Pharmaceutical Sciences The Fifth Affiliated Hospital Guangzhou Medical University Guangzhou PR China
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  fullname: Liu, Zumei
  organization: Guangdong Second Provincial General Hospital
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  givenname: Zhimin
  surname: Gao
  fullname: Gao, Zhimin
  organization: Guangzhou Medical University
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  givenname: Lihuan
  surname: Zeng
  fullname: Zeng, Lihuan
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  surname: Wu
  fullname: Wu, Xiaoqian
  email: wuxiaoqian@gzhmu.edu.cn
  organization: Guangzhou Medical University
BackLink https://www.ncbi.nlm.nih.gov/pubmed/33660406$$D View this record in MEDLINE/PubMed
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Issue 2
Keywords apoptosis
nobiletin
hypertrophy
acute myocardial infarction
cardiac remodeling
Language English
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Notes Zumei Liu, Zhimin Gao and Lihuan Zeng authors are contributed equally to this work.
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e_1_2_9_27_1
e_1_2_9_48_1
Zhao Y‐S (e_1_2_9_44_1) 2019; 2019
e_1_2_9_29_1
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Snippet Nobiletin was found to protect against acute myocardial infarction (AMI)‐induced cardiac function decline and myocardial remodeling, although the dose–effect...
Nobiletin was found to protect against acute myocardial infarction (AMI)-induced cardiac function decline and myocardial remodeling, although the dose-effect...
Abstract Nobiletin was found to protect against acute myocardial infarction (AMI)‐induced cardiac function decline and myocardial remodeling, although the...
Abstract Nobiletin was found to protect against acute myocardial infarction (AMI)‐induced cardiac function decline and myocardial remodeling, although the...
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SubjectTerms acute myocardial infarction
Animals
Apoptosis
Apoptosis - drug effects
Autophagy
cardiac remodeling
Cardiotonic Agents - pharmacology
Cardiotonic Agents - therapeutic use
Cell Line
Coronary vessels
Disease Models, Animal
Dose-Response Relationship, Drug
Flavones - pharmacology
Flavones - therapeutic use
Gene expression
Glucose
Heart attacks
Humans
hypertrophy
Ischemia
JNK Mitogen-Activated Protein Kinases - antagonists & inhibitors
JNK Mitogen-Activated Protein Kinases - metabolism
Kinases
Laboratory animals
Male
MAP Kinase Signaling System - drug effects
Medical research
Myoblasts - drug effects
Myoblasts - pathology
Myocardial Infarction - complications
Myocardial Infarction - drug therapy
Myocardial Infarction - pathology
Myocardium - cytology
Myocardium - pathology
nobiletin
Original
Ostomy
Pharmacology
Phosphorylation
Proteins
Rats
Ventricular Remodeling - drug effects
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Title Nobiletin ameliorates cardiac impairment and alleviates cardiac remodeling after acute myocardial infarction in rats via JNK regulation
URI https://onlinelibrary.wiley.com/doi/abs/10.1002%2Fprp2.728
https://www.ncbi.nlm.nih.gov/pubmed/33660406
https://www.proquest.com/docview/2511006498
https://www.proquest.com/docview/2570158390
https://www.proquest.com/docview/2497097417/abstract/
https://pubmed.ncbi.nlm.nih.gov/PMC7931132
https://doaj.org/article/4a34f3276c854043abd3494b0aa02c7d
Volume 9
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