Authors

Xiao Yun*, Yuanfeng Zhang**, Xianju Zhou***, Huifang Yun**,#

Departments

*Department of Hepatobiliary Surgery, The Affiliated Changzhou No.2 People’s Hospital of Nanjing Medical University, Changzhou, Jiangsu, China - **Department of Anesthesiology, The Affiliated Changzhou No.2 People’s Hospital of Nanjing Medical University, Changzhou, Jiangsu, China - ***Laboratory of Neurological Diseases, Department of Neurology, The Affiliated Changzhou No.2 People’s Hospital of Nanjing Medical University, Changzhou, Jiangsu, China

Abstract

Objective: To study the effect of ulinastatin (UTI) on myocardial ischemia-reperfusion injury (MIRI) through extracellular signal-regulated kinase (ERK) signaling pathway. 

Materials and methods: 24 Sprague-Dawley rats were randomly divided into sham group (n = 8), IR group (n =8), UTI group (n =8) to establish MIRI rat model. The changes of serum biochemical indexes, including SOD (SOD) and MDA (MDA), were detected by kit. The changes of serum inflammatory factor expression, including interleukin-6 (IL-6) and tumor necrosis factor-α (TNF-α), were detected by quantitative reverse transcription-polymerase chain reaction (qRT-PCR) and enzyme-linked immunosorbent assay (ELISA). The phosphorylation level of ERK and the expression of cleaved caspase-3 were detected by qRT-PCR and Western blot methods. 

Results: Compared with sham group, SOD content in I/R group significantly decreased (p<0.01), MDA content significantly increased (p<0.01), and UTI group significantly improved (p<0.01).The results of qRT-PCR and ELISA kit showed that the inflammatory factors (IL-6 and TNF-α) in UTI group were significantly increased (p<0.01). The results of qRT-PCR and Western blotting showed that the phosphorylation level of ERK and the expression of cleaved caspase-3 in UTI group were significantly improved (p<0.01). 

Conclusion: UTI can play a protective role in MIRI by up-regulating ERK signaling pathway. 

Keywords

Ulinastatin, ERK, myocardial ischemia-Rreperfusion injury.

DOI:

10.19193/0393-6384_2019_6_501