PMID- 31389586
OWN - NLM
STAT- MEDLINE
DCOM- 20200611
LR  - 20200611
IS  - 2284-0729 (Electronic)
IS  - 1128-3602 (Linking)
VI  - 23
IP  - 3 Suppl
DP  - 2019 Jan
TI  - Cardioprotective effect of erythropoietin in rats with acute myocardial 
      infarction through JNK pathway.
PG  - 153-160
LID - 18642 [pii]
LID - 10.26355/eurrev_201901_18642 [doi]
AB  - OBJECTIVE: To explore the molecular mechanism of the cardioprotective effect of 
      erythropoietin (EPO) in the rats with acute myocardial infarction (AMI) via the 
      c-Jun N-terminal kinase (JNK) pathway. MATERIALS AND METHODS: The rat AMI models 
      were constructed and randomly divided into the EPO group, AMI group, and Sham 
      group. At 2 weeks after successful modeling, the cardiac function-related 
      indicators of rats were determined, and after the rats were sacrificed, the left 
      ventricular weight (LVW) index was measured. The enzyme-linked immunosorbent 
      assay (ELISA) and the terminal deoxynucleotidyl transferase-mediated dUTP nick 
      end labeling (TUNEL) assay were employed to determine the levels of the related 
      serum inflammatory factors and myocardial apoptosis, respectively. The apoptosis 
      and the expression levels of the JNK pathway-related messenger ribonucleic acids 
      (mRNA) and proteins in the myocardial tissues of all groups of rats were 
      determined via Real Time-Polymerase Chain Reaction (RT-PCR) and 
      immunohistochemistry. RESULTS: After intervention with EPO, the EPO group had a 
      substantially lower left ventricular end-diastolic pressure, but a remarkably 
      higher left ventricular systolic pressure than the AMI group (p<0.05), and the 
      LVW and LVW/body weight (BW) notably declined in the EPO group compared with 
      those in AMI group (p<0.05). According to the ELISA results, the inflammatory 
      factors were substantially raised in the AMI group compared with those in the 
      other two groups (p<0.05) and significantly lowered after treatment with EPO 
      (p<0.05). The TUNEL assay results revealed that EPO treatment could reverse the 
      pathological changes in AMI to decrease the apoptosis to a large extent. It was 
      detected via RT-PCR and immunohistochemistry that, compared with those in the 
      Sham group, the expression level of the anti-apoptosis gene B-cell lymphoma 2 
      (Bcl-2) was substantially decreased, but the expression levels of pro-apoptosis 
      gene Bcl-2 associated X protein (Bax) and the JNK pathway-related JNK and c-Jun 
      were evidently elevated in the AMI group (p<0.05). Moreover, the expression level 
      of Bcl-2 was remarkably raised (p<0.05) and the expression levels of Bax, JNK, 
      and c-Jun remarkably declined (p<0.05) in the EPO group after intervention with 
      EPO. CONCLUSIONS: EPO can inhibit the inflammatory responses and decrease the 
      myocardial apoptosis to protect the heart of the AMI rats, and its mechanism of 
      action is related to the inhibition of the expression of the JNK pathway.
FAU - Li, G-Q
AU  - Li GQ
AD  - Department of Cardiology, Heze Municipal Hospital, Heze, China. lgq2020@sohu.com.
FAU - Chen, M
AU  - Chen M
LA  - eng
PT  - Journal Article
PL  - Italy
TA  - Eur Rev Med Pharmacol Sci
JT  - European review for medical and pharmacological sciences
JID - 9717360
RN  - 0 (Bax protein, rat)
RN  - 0 (Bcl2 protein, rat)
RN  - 0 (Cardiotonic Agents)
RN  - 0 (Proto-Oncogene Proteins c-bcl-2)
RN  - 0 (Proto-Oncogene Proteins c-jun)
RN  - 0 (bcl-2-Associated X Protein)
RN  - 11096-26-7 (Erythropoietin)
RN  - EC 2.7.11.24 (JNK Mitogen-Activated Protein Kinases)
SB  - IM
MH  - Animals
MH  - Apoptosis
MH  - Cardiotonic Agents/*pharmacology
MH  - Enzyme-Linked Immunosorbent Assay
MH  - Erythropoietin/*pharmacology
MH  - In Situ Nick-End Labeling
MH  - JNK Mitogen-Activated Protein Kinases/*metabolism
MH  - MAP Kinase Signaling System/*drug effects
MH  - Male
MH  - Myocardial Infarction/*prevention & control
MH  - Myocardium/pathology
MH  - Proto-Oncogene Proteins c-bcl-2/metabolism
MH  - Proto-Oncogene Proteins c-jun/metabolism
MH  - Rats
MH  - Rats, Sprague-Dawley
MH  - bcl-2-Associated X Protein/metabolism
EDAT- 2019/08/08 06:00
MHDA- 2020/06/12 06:00
CRDT- 2019/08/08 06:00
PHST- 2019/08/08 06:00 [entrez]
PHST- 2019/08/08 06:00 [pubmed]
PHST- 2020/06/12 06:00 [medline]
AID - 18642 [pii]
AID - 10.26355/eurrev_201901_18642 [doi]
PST - ppublish
SO  - Eur Rev Med Pharmacol Sci. 2019 Jan;23(3 Suppl):153-160. doi: 
      10.26355/eurrev_201901_18642.