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Effect of SecinH3 on lung injury induced by sepsis of rats
1Intensive Care Unit, Sir Run Run Shaw Hospital, School of Medicine, Zhejiang University, Hangzhou 310016, China.
Objective:
To study effect of SecinH3 on lung injury induced by the sepsis of rats.
Methods:
A total of 30 SPF Wistar rats were randomly divided into two groups, including 5 rats in the control group and 25 in the model group. The intraperitoneal injection of endotoxin-lipopolysaccharide (LPS) was performed to build the animal model of sepsis. The blood gas analysis was carried out. Afterwards, change in the expression of pro-inflammatory factors of IL-1, IL-6 and TNF-α in the serum were detected. To study the mechanism of SecinH3 in the process of lung injury induced by the sepsis, the rats with the successful modeling of sepsis were randomly divided into two groups. Rats in the SecinH3 group were given the intraperitoneal injection of 100 μg/12 h SecinH3 for 24 h; while rats in the control group were given the injection of same solvent by the same dosage. The blood was drawn from the heart by 500 μL for the blood gas analysis to detect the change in the expression of pro-inflammatory factors of IL-1, IL-6 and TNF-α in the treatment group and control group. After separating the lung tissue, the Real-time PCR and western blotting were performed to analyze the effect of SecinH3 on the expression of cytohesins and also discuss the change of epidermal growth factor receptor (EGFR) and p-EGFR related to the signaling pathway of EGFR-p38 mitogen-activated protein kinase that is regulated by cytohesins.
Results:
Three rats died within 4 h after the injection of LPS, while other 22 ones had the successful modeling, with the success rate of 88%. After being stimulated by LPS, compared with the control group, the arterial partial pressure of oxygen of rats in the treatment group was significantly reduced (P < 0.05), while the partial pressure of CO2 was significantly increased (P < 0.01). After being treated by SecinH3, Pa/O2 was increased with the sepsis, while Pa/CO2 was decreased with the action of SecinH3, which indicated that SecinH3 had the certain 'repairing' ability for the lung injury. SecinH3 might inhibit the cytohesins and then inhibit the phosphorylation of EGFR.
Conclusions:
SecinH3 can significantly inhibit the cytohesins and then relieve the lung injury induced by the sepsis of rats.
