Effect of dexmedetomidine pretreatment on JAK/STAT signaling pathway during myocardial injury induced by liver ischemia-reperfusion in rats
10.3760/cma.j.issn.0254-1416.2019.01.011
- VernacularTitle:右美托咪定预先给药对肝缺血再灌注致大鼠心肌损伤时JAK/STAT信号通路的影响
- Author:
Hongxia LI
1
;
Yiqi WENG
;
Wenli YU
;
Shaoting YUAN
;
Lili JIA
;
Fei WANG
Author Information
1. 天津市第一中心医院麻醉科 300192
- Keywords:
Dexmedetomidine;
Reperfusion injury;
Liver;
Myocardium;
Janus kinase;
Activating transcription factor
- From:
Chinese Journal of Anesthesiology
2019;39(1):44-47
- CountryChina
- Language:Chinese
-
Abstract:
Objective To investigate the effect of dexmedetomidine pretreatment on Janus kinase/signal transducer and activator of transcription (JAK/STAT) signaling pathway during myocardial injury induced by liver ischemia-reperfusion (I/R) in rats.Methods Twenty-four healthy adult male SpragueDawley rats,aged 8-10 weeks,weighing 220-250 g,were divided into 3 groups (n=8 each) using a random number table method:sham operation group (group S),liver I/R group (group I/R),and dexmedetomidine pretreatment group (group D).The portal vein,superior and inferior vena cava,subhepatic inferior vena cava and hepatic artery were clamped,and the liver was perfused with 4 ℃ lactated Ringer's solution for 60 min through the portal vein to establish the model of liver cold I/R in anesthetized rats.Dexmedetomidine 100 μg/kg was intraperitoneally injected at 30 min before ischemia in group D.Blood samples were collected at 8 h of reperfusion from the inferior vena cava for determination of serum cardiac troponin Ⅰ (cTnⅠ) and heart-type fatty acid binding protein (H-FABP) concentrations (using the automatic biochemistry analyzer),tumor necrosis factor-alpha (TNF-α) and high-mobility group box 1 protein (HMGB1) concentrations (by enzyme-linked immunosorbent assay).The rats were then sacrificed,andhearts were harvested for examination of histopathological changes (with a light microscope) and for determination of the malondialdehyde (MDA) content (using thiobarbituric acid method) and superoxide dismutase (SOD) activity (by xanthine oxidase method),and expression of phosphorylated STAT1 and STAT3 (p-STAT1,p-STAT3) and phosphorylated JAK2 (p-JAK2) in myocardial tissues (by Western blot).Results Compared with group S,the serum concentrations of cTnI,H-FABP,TNF-α and HMGB1 were significantly increased,the MDA content was increased,the SOD activity was decreased,and the expression of p-JAK2,p-STAT1 and p-STAT3 was up-regulated in I/R and D groups (P＜0.05).Compared with group I/R,the serum concentrations of cTnI,H-FABP,TNF-α and HMGB1 were significantly decreased,the MDA content was decreased,the SOD activity was increased,the expression of pJAK2,p-STAT1 and p-STAT3 was down-regulated (P＜0.05),and pathological changes of myocardium were significantly attenuated in group D.Conclusion The mechanism by which dexmedetomidine pretreatment mitigates myocardial injury induced by liver cold I/R may be related to inhibiting activation of JAK/STAT signaling pathway in rats.
