PMID- 31002169
OWN - NLM
STAT- MEDLINE
DCOM- 20200908
LR  - 20200908
IS  - 2284-0729 (Electronic)
IS  - 1128-3602 (Linking)
VI  - 23
IP  - 7
DP  - 2019 Apr
TI  - Effect of IL-6-mediated STAT3 signaling pathway on myocardial apoptosis in mice 
      with dilated cardiomyopathy.
PG  - 3042-3050
LID - 17586 [pii]
LID - 10.26355/eurrev_201904_17586 [doi]
AB  - OBJECTIVE: To investigate the effect of interleukin-6 (IL-6) gene knockout on 
      apoptosis of myocardial cells in mice with Coxsackievirus B3 (CVB3)-induced 
      dilated cardiomyopathy (DCM) and its potential mechanism, so as to provide 
      certain references for the clinical prevention and treatment of DCM. MATERIALS 
      AND METHODS: A total of 40 male C57 mice were randomly divided into Sham group 
      (n=20) and DCM group (n=20) using a random number table. Another 20 mice with 
      IL-6 gene knockout were enrolled into DCM+IL-6 KO group (n=20). The DCM model was 
      established via CVB3 repeated incremental infection. After 9 months, the heart 
      weight/body weight (HW/BW) ratio of mice in each group was detected. The ejection 
      fraction [EF (%)] and fraction shortening [FS (%)] of mice in each group were 
      detected via two-dimensional ultrasonography. The cross-sectional area and 
      pathological changes in myocardial cells in the heart in each group were 
      determined using hematoxylin-eosin (HE) staining. The collagen content in 
      myocardial tissues in each group was detected via Masson staining and picrosirius 
      red (PSR) staining, and the expressions of Collagen I and Collagen III in 
      myocardial tissues in each group were detected via immunohistochemistry. In 
      addition, the myocardial apoptosis in myocardial tissues in each group was 
      detected via terminal deoxynucleotidyl transferase-mediated dUTP nick end 
      labeling (TUNEL) staining. Finally, the protein expression levels of B-cell 
      lymphoma-2 (Bcl-2), Bcl-2 associated X protein (Bax), phosphorylated signal 
      transducer and activator of transcription 3 (p-STAT3), and total STAT3 (t-STAT3) 
      were detected via Western blotting. RESULTS: The expression of IL-6 messenger 
      ribonucleic acids (mRNAs) in myocardial tissues in DCM group was significantly 
      increased compared with that in Sham group (p<0.05). After IL-6 knockout, the 
      HW/BW ratio of DCM mice significantly declined (p<0.05), and the cross-sectional 
      area of myocardial cells was significantly reduced (p<0.05). According to the 
      results of echocardiography, the cardiac function of mice in DCM+IL-6 KO group 
      was significantly superior to that in DCM group, manifested as the significant 
      increase in FS (%) and EF (%) (p<0.05). The results of Masson staining, PSR 
      staining, and immunohistochemical staining showed that IL-6 knockout could reduce 
      the collagen content and Collagen I and Collagen III expressions in myocardial 
      tissues of DCM mice (p<0.05). Furthermore, it was found via TUNEL staining that 
      the number of apoptotic myocardial cells in DCM+IL-6 KO group was markedly 
      smaller than that in DCM group (p<0.05). At the same time, the Bax/Bcl-2 ratio in 
      myocardial tissues in DCM+IL-6 KO group was lower (p<0.05). Finally, the results 
      of Western blotting revealed that DCM+IL-6 KO group had a lower phosphorylation 
      level of STAT3 than DCM group (p<0.05). CONCLUSIONS: Inhibiting IL-6 gene may 
      improve the DCM-induced myocardial remodeling through reducing myocardial 
      apoptosis.
FAU - Li, Q
AU  - Li Q
AD  - Department of Geriatrics, Quanzhou First Hospital of Fujian Medical University, 
      Quanzhou, China. drheyafeng@foxmail.com.
FAU - Ye, W-X
AU  - Ye WX
FAU - Huang, Z-J
AU  - Huang ZJ
FAU - Zhang, Q
AU  - Zhang Q
FAU - He, Y-F
AU  - He YF
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 (Interleukin-6)
RN  - 0 (STAT3 Transcription Factor)
RN  - 0 (Stat3 protein, mouse)
SB  - IM
MH  - Animals
MH  - Apoptosis/*physiology
MH  - Cardiomyopathy, Dilated/genetics/*metabolism/*pathology
MH  - Interleukin-6/*deficiency/genetics
MH  - Male
MH  - Mice
MH  - Mice, Inbred C57BL
MH  - Mice, Knockout
MH  - STAT3 Transcription Factor/genetics/*metabolism
MH  - Signal Transduction/*physiology
MH  - Ventricular Remodeling/physiology
EDAT- 2019/04/20 06:00
MHDA- 2020/09/09 06:00
CRDT- 2019/04/20 06:00
PHST- 2019/04/20 06:00 [entrez]
PHST- 2019/04/20 06:00 [pubmed]
PHST- 2020/09/09 06:00 [medline]
AID - 17586 [pii]
AID - 10.26355/eurrev_201904_17586 [doi]
PST - ppublish
SO  - Eur Rev Med Pharmacol Sci. 2019 Apr;23(7):3042-3050. doi: 
      10.26355/eurrev_201904_17586.