Remote Ischemic Postconditioning Protects against Myocardial Ischemia-Reperfusion Injury by Inhibition of the RAGE-HMGB1 Pathway

Autor: Xiangming Wang, Zakaria Iyan, Zhijian Yang, Yan Guo, Junhong Wang, Tiantian Tu, Deeraj Mungun
Jazyk: angličtina
Rok vydání: 2018
Předmět:
0301 basic medicine
Male
medicine.medical_specialty
Article Subject
Receptor for Advanced Glycation End Products
Ischemia
Infarction
lcsh:Medicine
Myocardial Reperfusion Injury
030204 cardiovascular system & hematology
medicine.disease_cause
HMGB1
General Biochemistry
Genetics and Molecular Biology
03 medical and health sciences
chemistry.chemical_compound
Mice
0302 clinical medicine
Internal medicine
Medicine
Animals
cardiovascular diseases
HMGB1 Protein
Ischemic Postconditioning
PI3K/AKT/mTOR pathway
Evans Blue
General Immunology and Microbiology
biology
business.industry
Akt/PKB signaling pathway
lcsh:R
General Medicine
medicine.disease
Mice
Inbred C57BL
Disease Models
Animal
030104 developmental biology
chemistry
Cardiology
biology.protein
business
Reperfusion injury
Oxidative stress
Signal Transduction
Research Article
Zdroj: BioMed Research International, Vol 2018 (2018)
BioMed Research International
ISSN: 2314-6141
2314-6133
Popis: Background. The aim of the present study was to observe the effect of RAGE-HMGB1 signal pathway on remote ischemic postconditioning in mice with myocardial ischemia reperfusion injury.Methods.Mice model of MIRI was established and randomly divided into three groups: control group, ischemia reperfusion group, and remote ischemic postconditioning group. Infarction size was detected by Evans blue and TTC staining. Cardiac function was detected by echocardiography measurement. The protein levels of RAGE, HMGB1, P-AKT, and ERK1/2 were detected by Western blot 120 min following reperfusion.Results.RIPostC could decrease the infarct size and increase LVEF and FS compared with I/R group. Two hours after myocardial ischemia reperfusion, the levels of RAGE and HMGB1 were significantly decreased in RIPostC group compared with those in I/R group. The level of p-AKT was significantly higher in the RIPostC group than in the I/R group. LY294002 significantly attenuated RIPostC-increased levels of Akt phosphorylation.Conclusion.RIPostC may inhibit the expression of RAGE and HMGB1 and activate PI3K/Akt signaling pathway to extenuate ischemic reperfusion injury in mice. It could further suppress the oxidative stress, have antiapoptosis effect, and reduce inflammatory reaction, but this effect has certain timeliness.
Databáze: OpenAIRE
Externí odkaz:
Nepřihlášeným uživatelům se plný text nezobrazuje