PMID- 33378040
OWN - NLM
STAT- MEDLINE
DCOM- 20210630
LR  - 20210630
IS  - 2284-0729 (Electronic)
IS  - 1128-3602 (Linking)
VI  - 24
IP  - 24
DP  - 2020 Dec
TI  - MiR-506 alleviates myocardial ischemia-reperfusion injury via targeting PI3K/AKT.
PG  - 12896-12903
LID - 24193 [pii]
LID - 10.26355/eurrev_202012_24193 [doi]
AB  - OBJECTIVE: The aim of this study was to explore the effects of micro ribonucleic 
      acid (miR)-506 and phosphatidylinositol 3-hydroxy kinase (PI3K)/protein kinase B 
      (AKT) pathway on myocardial ischemia-reperfusion injury (MIRI) in rats. MATERIALS 
      AND METHODS: A total of 90 healthy rats weighing 260-300 g were selected as 
      research subjects, and divided into three groups, including: Control group 
      (n=30), IR group (n=30), and miRNA treatment group (IR + miR-506 group, n=30). 
      The model was successfully established via threading the coronary artery. The 
      structural differences in myocardial tissues were observed via hematoxylin-eosin 
      (HE) staining in each group. The mRNA expressions of miR-506 and PI3K in 
      myocardial tissues were detected using fluorescence quantitative Polymerase Chain 
      Reaction (qPCR). Meanwhile, AKT protein phosphorylation activity in myocardial 
      tissues was detected as well. The apoptosis of myocardial tissues was detected 
      via terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL) 
      staining. In addition, superoxide dismutase (SOD) activity and malondialdehyde 
      (MDA) content in myocardial tissues were compared in each group. RESULTS: In 
      Control group, no structural abnormalities were found in myocardial tissues, and 
      no inflammatory cells were observed. In IR group, myocardial tissues were 
      arranged disorderly, and inflammatory cell infiltration was found. In IR + 
      miR-506 group, myocardial tissue lesions were milder than those in the IR group. 
      qPCR results indicated that the mRNA expressions of miR-506 and PI3K in 
      myocardial tissues were statistically different among groups (p<0.05), with the 
      lowest in the IR group. The expression of miR-506 was evidently higher in IR + 
      miR-506 group than that in the Control group (p<0.05). However, the mRNA 
      expression of PI3K was significantly higher in the Control group than IR + 
      miR-506 group (p<0.05). There was a significant positive correlation between the 
      expressions of miR-506 and PI3K in each group (p<0.05). The phosphorylation 
      activity of AKT protein in IR + miR-506 group was markedly higher than the other 
      two groups (p<0.05). In addition, TUNEL staining demonstrated that the apoptosis 
      rate in Control group, IR group and IR + miR-506 group was only 1.3%, 20.3%, and 
      9.8%, respectively. SOD activity was remarkably stronger in the Control group 
      (62.7 U/mg pro) than the other two groups (p<0.05). In addition, MDA content was 
      remarkably higher in IR group (0.747 nmol/mg pro) than that in the other two 
      groups (p<0.05). CONCLUSIONS: MiR-506 is associated with myocardial injury in 
      rats, which can alleviate myocardial injury through the PI3K/AKT signaling 
      pathway.
FAU - Zhang, M
AU  - Zhang M
AD  - Department of Anesthesiology, The Affiliated Huaian No. 1 People's Hospital of 
      Nanjing Medical University, Huaian, China. hayyzhm@njmu.edu.cn.
FAU - Wang, J-Y
AU  - Wang JY
FAU - Li, L
AU  - Li L
FAU - Li, G-M
AU  - Li GM
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 (MicroRNAs)
RN  - EC 2.7.11.1 (Proto-Oncogene Proteins c-akt)
SB  - IM
MH  - Animals
MH  - Disease Models, Animal
MH  - MicroRNAs/genetics/*metabolism
MH  - Myocardial Reperfusion Injury/*metabolism/pathology
MH  - Phosphatidylinositol 3-Kinases/*metabolism
MH  - Proto-Oncogene Proteins c-akt/*metabolism
MH  - Rats
MH  - Signal Transduction
EDAT- 2020/12/31 06:00
MHDA- 2021/07/01 06:00
CRDT- 2020/12/30 12:42
PHST- 2020/12/30 12:42 [entrez]
PHST- 2020/12/31 06:00 [pubmed]
PHST- 2021/07/01 06:00 [medline]
AID - 24193 [pii]
AID - 10.26355/eurrev_202012_24193 [doi]
PST - ppublish
SO  - Eur Rev Med Pharmacol Sci. 2020 Dec;24(24):12896-12903. doi: 
      10.26355/eurrev_202012_24193.