title: RP105 protects against myocardial ischemia-reperfusion injury via suppressing TLR4 signaling pathways in rat model.
abstract: Myocardial ischemia-reperfusion (I/R) injury severely impacts the postoperative survival rate of coronary atherosclerotic heart disease. Radioprotective 105 kDa protein (RP105) is a regulator of Toll-like receptor 4 (TLR4), an inflammatory factor whose functions have been reported in myocardial I/R injury. To investigate the roles of RP105 in mediating myocardial I/R injury, we overexpressed RP105 by injecting its adenovirus vectors, and induced myocardial I/R injury rat model in this study. Myocardial structure injuries of rat hearts were examined by hematoxylin eosin staining, and myocardial infarct area was calculated after Evans blue and triphenyltetrazolium chloride dual staining. Expression changes of TLR4, myeloid differentiation factor 88 (MyD88), and nuclear factor κB (NF-κB) in myocardia were detected by quantitative real-time PCR and Western blot. Amount changes of tumor necrosis factor α (TNF-α) and interleukin-6 (IL-6) were detected by enzyme-linked immunosorbent assay. Results showed that RP105 attenuated myocardial injuries and effectively reduced myocardial infarct area after I/R (P<0.05). RP105 was also proved to significantly inhibit TLR4 and downstream inflammatory factors MyD88, NF-κB, TNF-α and IL-6 (P<0.05), whose expression levels were up-regulated by I/R induction. These results indicated that RP105 could protect against myocardial I/R injury via suppressing inflammatory responses mediated by TLR4 signaling pathways. This study revealed the anti-inflammatory roles of RP105 and its potential in preventing and treating myocardial I/R injury.
authors.affiliation: Department of Cardiology, the First College of Clinical Medical Sciences, China Three Gorges University, Yichang, Hubei 443000, China; Department of Cardiology, Yichang Central People's Hospital, Yichang, Hubei 443000, China.
authors.forename: Xinxin
authors.initials: X
authors.lastname: Li
authors.affiliation: Department of Cardiology, the First College of Clinical Medical Sciences, China Three Gorges University, Yichang, Hubei 443000, China; Department of Cardiology, Yichang Central People's Hospital, Yichang, Hubei 443000, China. Electronic address: yangjun3382@126.com.
authors.forename: Jun
authors.initials: J
authors.lastname: Yang
authors.affiliation: Department of Cardiology, the First College of Clinical Medical Sciences, China Three Gorges University, Yichang, Hubei 443000, China; Department of Cardiology, Yichang Central People's Hospital, Yichang, Hubei 443000, China.
authors.forename: Jian
authors.initials: J
authors.lastname: Yang
authors.affiliation: Department of Cardiology, the First College of Clinical Medical Sciences, China Three Gorges University, Yichang, Hubei 443000, China; Department of Cardiology, Yichang Central People's Hospital, Yichang, Hubei 443000, China.
authors.forename: Wusong
authors.initials: W
authors.lastname: Dong
authors.affiliation: Department of Cardiology, the First College of Clinical Medical Sciences, China Three Gorges University, Yichang, Hubei 443000, China; Department of Cardiology, Yichang Central People's Hospital, Yichang, Hubei 443000, China.
authors.forename: Song
authors.initials: S
authors.lastname: Li
authors.affiliation: Department of Cardiology, the First College of Clinical Medical Sciences, China Three Gorges University, Yichang, Hubei 443000, China; Department of Cardiology, Yichang Central People's Hospital, Yichang, Hubei 443000, China.
authors.forename: Hui
authors.initials: H
authors.lastname: Wu
authors.affiliation: Department of Cardiology, the First College of Clinical Medical Sciences, China Three Gorges University, Yichang, Hubei 443000, China; Department of Cardiology, Yichang Central People's Hospital, Yichang, Hubei 443000, China.
authors.forename: Li
authors.initials: L
authors.lastname: Li
mesh_terms: D000256:Adenoviridae / Q000235:genetics; D000818:Animals; D015153:Blotting, Western; D004195:Disease Models, Animal; D004797:Enzyme-Linked Immunosorbent Assay; D015870:Gene Expression; D015316:Genetic Therapy / Q000379:methods; D005822:Genetic Vectors / Q000235:genetics; D015850:Interleukin-6 / Q000378:metabolism; D008297:Male; D053594:Myeloid Differentiation Factor 88 / Q000235:genetics / Q000378:metabolism; D009203:Myocardial Infarction / Q000235:genetics / Q000378:metabolism / Q000628:therapy; D015428:Myocardial Reperfusion Injury / Q000235:genetics* / Q000378:metabolism / Q000628:therapy; D009206:Myocardium / Q000378:metabolism / Q000473:pathology; D016328:NF-kappa B / Q000235:genetics / Q000378:metabolism; D017207:Rats, Sprague-Dawley; D020133:Reverse Transcriptase Polymerase Chain Reaction; D015398:Signal Transduction / Q000235:genetics*; D051197:Toll-Like Receptor 4 / Q000235:genetics* / Q000378:metabolism; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism
chemical_list: D015850:Interleukin-6; C507781:Myd88 protein, rat; D053594:Myeloid Differentiation Factor 88; D016328:NF-kappa B; D051197:Toll-Like Receptor 4; D014409:Tumor Necrosis Factor-alpha
keywords: Inflammatory factors; Myocardial ischemia–reperfusion injury; Radioprotective 105kDa protein (RP105); Toll-like receptor 4 (TLR4)