PMID- 33275272
OWN - NLM
STAT- MEDLINE
DCOM- 20210629
LR  - 20210629
IS  - 2284-0729 (Electronic)
IS  - 1128-3602 (Linking)
VI  - 24
IP  - 22
DP  - 2020 Nov
TI  - Ghrelin inhibits inflammatory response and apoptosis of myocardial injury in 
      septic rats through JAK/STAT signaling pathway.
PG  - 11740-11746
LID - 23825 [pii]
LID - 10.26355/eurrev_202011_23825 [doi]
AB  - OBJECTIVE: The purpose of this study was to explore the influence of Ghrelin on 
      myocardial injury of septic rats through the Janus kinase/signal transducer and 
      activator of transcription (JAK/STAT) signaling pathway. MATERIALS AND METHODS: A 
      total of 36 Sprague-Dawley rats were randomly divided into normal group (n=12), 
      model group (n=12), and Ghrelin group (n=12). The rats in the normal group were 
      fed normally, while those in the model group were intraperitoneally injected with 
      endotoxin to establish the sepsis model. The rats in the Ghrelin group were given 
      intraperitoneal injection of Ghrelin solution to prepare the sepsis model. 9 h 
      later, the specimens were obtained. Then, the expressions of interleukin-6 (IL-6) 
      and tumor necrosis factor-alpha (TNF-alpha) were detected via immunohistochemistry, 
      and the protein expressions of phosphorylated JAK (p-JAK) and STAT3 were 
      determined by Western blotting (WB). Next, enzyme-linked immunosorbent assay 
      (ELISA) was performed to measure the content of IL-6 and TNF-alpha, and quantitative 
      Polymerase Chain Reaction (qPCR) was applied to examine the messenger ribonucleic 
      acid (mRNA) expressions of JAK and STAT3. Finally, the cell apoptosis was 
      detected through terminal deoxynucleotidyl transferase-mediated dUTP nick end 
      labeling (TUNEL) assay. RESULTS: The results of immunohistochemistry showed that 
      compared with those in the normal group, the positive expression levels of IL-6 
      and TNF-alpha were markedly increased in other groups (p<0.05), while in comparison 
      with those in the model group, the positive expression levels of IL-6 and TNF-alpha 
      were decreased significantly in the Ghrelin group (p<0.05). The WB results 
      indicated that the model group and Ghrelin group had remarkably higher protein 
      expression levels of p-JAK and STAT3 than the normal group (p<0.05), and Ghrelin 
      group exhibited notably lower protein expression levels of p-JAK and STAT3 than 
      the model group (p<0.05). According to the results of qPCR, the relative mRNA 
      expression levels of JAK and STAT3 were distinctly raised in the model group and 
      Ghrelin group in comparison with those in the normal group (p<0.05), while they 
      were reduced evidently in the Ghrelin group compared with those in the model 
      group (p<0.05). Furthermore, it was manifested in the results of ELISA that the 
      model group and Ghrelin group had prominently elevated content of TNF-alpha and IL-6 
      compared with normal group (p<0.05), and Ghrelin group displayed significantly 
      lowered content of TNF-alpha and IL-6 in comparison with the model group (p<0.05). 
      Moreover, the TUNEL results revealed that the apoptosis rate was remarkably 
      higher in the other two groups than that in the normal group (p<0.05), while it 
      was evidently lower in the Ghrelin group than that in the model group (p<0.05). 
      CONCLUSIONS: Ghrelin can inhibit inflammatory response and apoptosis in the 
      process of myocardial injury in septic rats by repressing the JAK/STAT signaling 
      pathway.
FAU - Jin, L
AU  - Jin L
AD  - Department of Cardiovascular Surgery, Shanghai Changhai Hospital, The Second 
      Military Medical University, Shanghai, China. libailingchzh@163.com.
FAU - Cai, C-L
AU  - Cai CL
FAU - Lang, X-L
AU  - Lang XL
FAU - Li, B-L
AU  - Li BL
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 (Ghrelin)
RN  - 0 (Lipopolysaccharides)
RN  - 0 (STAT3 Transcription Factor)
RN  - 0 (STAT3 protein, human)
RN  - EC 2.7.10.2 (Janus Kinases)
SB  - IM
MH  - Animals
MH  - Apoptosis/*drug effects
MH  - Disease Models, Animal
MH  - Female
MH  - Ghrelin/administration & dosage/*pharmacology
MH  - Inflammation/chemically induced/*drug therapy/pathology
MH  - Injections, Intraperitoneal
MH  - Janus Kinases/metabolism
MH  - Lipopolysaccharides/administration & dosage
MH  - Male
MH  - Myocardial Reperfusion Injury/chemically induced/*drug therapy/pathology
MH  - Rats
MH  - Rats, Sprague-Dawley
MH  - STAT3 Transcription Factor/metabolism
MH  - Sepsis/chemically induced/*drug therapy/pathology
MH  - Signal Transduction/drug effects
EDAT- 2020/12/05 06:00
MHDA- 2021/06/30 06:00
CRDT- 2020/12/04 12:08
PHST- 2020/12/04 12:08 [entrez]
PHST- 2020/12/05 06:00 [pubmed]
PHST- 2021/06/30 06:00 [medline]
AID - 23825 [pii]
AID - 10.26355/eurrev_202011_23825 [doi]
PST - ppublish
SO  - Eur Rev Med Pharmacol Sci. 2020 Nov;24(22):11740-11746. doi: 
      10.26355/eurrev_202011_23825.