Dexmedetomidine improves acute stress‐induced liver injury in rats by regulating MKP‐1, inhibiting NF‐κB pathway and cell apoptosis

Autor: Xiujing Feng, Xueyuan Hu, Honggang Fan, Huayun Zhang, Jichen Sha, Bei Li, Yongping Chen
Rok vydání: 2019
Předmět:
0301 basic medicine
Physiology
p38 mitogen-activated protein kinases
Clinical Biochemistry
Apoptosis
Inflammation
Pharmacology
medicine.disease_cause
p38 Mitogen-Activated Protein Kinases
03 medical and health sciences
0302 clinical medicine
polycyclic compounds
medicine
Animals
Humans
Lung
Liver injury
chemistry.chemical_classification
Reactive oxygen species
Behavior
Animal
business.industry
JNK Mitogen-Activated Protein Kinases
NF-kappa B
Transcription Factor RelA
Dual Specificity Phosphatase 1
Cell Biology
medicine.disease
Rats
Oxidative Stress
030104 developmental biology
Liver
Terminal deoxynucleotidyl transferase
chemistry
030220 oncology & carcinogenesis
bcl-Associated Death Protein
Liver function
medicine.symptom
Reactive Oxygen Species
business
Dexmedetomidine
hormones
hormone substitutes
and hormone antagonists
Oxidative stress
Signal Transduction
Zdroj: Journal of Cellular Physiology. 234:14068-14078
ISSN: 1097-4652
0021-9541
DOI: 10.1002/jcp.28096
Popis: Acute stress is a frequent and unpredictable disease for many animals. Stress is widely considered to affect liver function. However, the underlying mechanism by which dexmedetomidine (DEX) attenuates acute stress-induced liver injury in rats remains unclear. In this study, we used forced swimming for 15 min and acute 3-hr restraint stress model. Behavioral tests and changes in norepinephrine levels confirmed the successful establishment of the acute stress model. Acute stress-induced liver injury, evidenced by hematoxylin and eosin-stained pathological sections and increased serum aminotransferase and aspartate aminotransferase levels, was reduced in DEX-treated livers. Reactive oxygen species and oxidative stress levels were dramatically decreased with DEX treatment compared with acute stress-induced liver injury. DEX significantly reduced acute stress-induced liver inflammation and apoptosis, as assessed by terminal deoxynucleotidyl transferase dUTP nick-end labeling staining and inflammation and apoptosis-related protein levels. DEX treatment also effectively inhibited acute stress-induced c-Jun N-terminal kinase (JNK), P38, and BAD signaling pathway activation, and significantly induced MKP-1 activation. Thus, DEX has a protective effect on acute-stress-induced liver injury by reducing inflammation and apoptosis, which suggests a potential clinical application for DEX in stress syndrome.
Databáze: OpenAIRE
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