title: Baicalin inhibits inflammation and attenuates myocardial ischaemic injury by aryl hydrocarbon receptor.
abstract: OBJECTIVE
  Recent evidence indicates that suppressing inflammation by specific drug target and treatment measures contributes to attenuate ischaemic injury and the related heart diseases. This study aimed to investigate the potential effect of baicalin on myocardial ischaemic injury through inhibition of inflammation by inactivating the aryl hydrocarbon receptor (AhR).
  
  
  METHODS
  The mouse model with myocardial ischaemic injury was prepared by the left anterior descending coronary artery-amputation and then treated using baicalin. After observing the expression of AhR by immunohistochemical staining, the AhR and inflammatory mediators in circulation and myocardial tissues, including high-sensitive C-reactive protein (hsCRP), interleukin (IL)-1β and IL-6, were detected based on enzyme-linked immunosorbent assay, real-time polymerase chain reaction and Western blot methods.
  
  
  RESULTS
  The results showed that (1) substantial expression of AhR was observed in myocardial tissues; (2) ischaemic injury caused myocardial necrosis and remodelling, and stimulated hsCRP, IL-1β and IL-6 by activation of AhR; and (3) baicalin alleviated the myocardial injury and inflammatory response by inhibiting the expression of AhR.
  
  
  CONCLUSIONS
  Our findings extend the list of AhR ligands beyond exogenous toxins and endogenous molecules to cardiac immunological factors, and moreover it could be considered potential drug targets due to its pathological modulatory properties, while baicalin demonstrated promise as a novel vehicle for ischaemic heart disease.
authors.affiliation: Cardiovascular Medicine Center, Affiliated Hospital of Guangdong Medical College, Zhanjiang, China.
authors.forename: Yiqiang
authors.initials: Y
authors.lastname: Xue
authors.affiliation: Laboratory of Vascular Surgery, Guangdong Medical College, Zhanjiang, China.
authors.forename: Xiaorong
authors.initials: X
authors.lastname: Shui
authors.affiliation: Department of Cardiovascular Medicine, The People's Hospital of Lianjiang, Zhanjiang, China.
authors.forename: Weiqing
authors.initials: W
authors.lastname: Su
authors.affiliation: Laboratory of Cardiovascular Diseases, Guangdong Medical College, Zhanjiang, China.
authors.forename: Yuan
authors.initials: Y
authors.lastname: He
authors.affiliation: Cardiovascular Medicine Center, Affiliated Hospital of Guangdong Medical College, Zhanjiang, China.
authors.forename: Xinlin
authors.initials: X
authors.lastname: Lu
authors.affiliation: Cardiovascular Medicine Center, Affiliated Hospital of Guangdong Medical College, Zhanjiang, China.
authors.forename: Yu
authors.initials: Y
authors.lastname: Zhang
authors.affiliation: Cardiovascular Medicine Center, Affiliated Hospital of Guangdong Medical College, Zhanjiang, China.|Laboratory of Cardiovascular Diseases, Guangdong Medical College, Zhanjiang, China.
authors.forename: Guosen
authors.initials: G
authors.lastname: Yan
authors.affiliation: Cardiovascular Medicine Center, Affiliated Hospital of Guangdong Medical College, Zhanjiang, China.
authors.forename: Shian
authors.initials: S
authors.lastname: Huang
authors.affiliation: Cardiovascular Medicine Center, Affiliated Hospital of Guangdong Medical College, Zhanjiang, China.|Laboratory of Cardiovascular Diseases, Guangdong Medical College, Zhanjiang, China.
authors.forename: Wei
authors.initials: W
authors.lastname: Lei
authors.affiliation: Cardiovascular Medicine Center, Affiliated Hospital of Guangdong Medical College, Zhanjiang, China.|Laboratory of Cardiovascular Diseases, Guangdong Medical College, Zhanjiang, China.
authors.forename: Can
authors.initials: C
authors.lastname: Chen
mesh_terms: D000818:Animals; D000893:Anti-Inflammatory Agents / Q000494:pharmacology*; D051792:Basic Helix-Loop-Helix Proteins / Q000037:antagonists & inhibitors* / Q000235:genetics / Q000378:metabolism; D002097:C-Reactive Protein / Q000378:metabolism; D004195:Disease Models, Animal; D005419:Flavonoids / Q000494:pharmacology*; D018836:Inflammation Mediators / Q000378:metabolism; D053583:Interleukin-1beta / Q000378:metabolism; D015850:Interleukin-6 / Q000378:metabolism; D008297:Male; D051379:Mice; D017202:Myocardial Ischemia / Q000235:genetics / Q000378:metabolism / Q000473:pathology / Q000517:prevention & control*; D009205:Myocarditis / Q000378:metabolism / Q000473:pathology / Q000517:prevention & control*; D032383:Myocytes, Cardiac / Q000187:drug effects* / Q000378:metabolism / Q000473:pathology; D009336:Necrosis; D018336:Receptors, Aryl Hydrocarbon / Q000037:antagonists & inhibitors* / Q000235:genetics / Q000378:metabolism; D015398:Signal Transduction / Q000187:drug effects; D020257:Ventricular Remodeling / Q000187:drug effects
chemical_list: D000893:Anti-Inflammatory Agents; D051792:Basic Helix-Loop-Helix Proteins; D002097:C-Reactive Protein; D005419:Flavonoids; D018836:Inflammation Mediators; D053583:Interleukin-1beta; D015850:Interleukin-6; D018336:Receptors, Aryl Hydrocarbon; C484722:Ahr protein, mouse; C587672:IL1B protein, mouse; C577686:interleukin-6, mouse; C038044:baicalin
keywords: aryl hydrocarbon receptor; baicalin; inflammation; ischaemic injury; myocardial necrosis