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: