大鼠脑出血致多器官功能障碍综合征模型血清内毒素与TNF-α mRNA基因表达的相关性研究

Objective To examine the relationship between gene expression of TNF-α mRNA and serum endotoxin of the rats following cerebral hemorrhage complicated by multiple organ dysfunction syndrome (CMODS) and to investigate the pathogenesis of CMODS. Methods 54 Wistar rats were randomly divided into nine groups: the normal control group (n=6), the sham-operative group (n=6), and the model group was induced in rats by injecting 0.8U collagenase into the caudase putamen (n=42). The content of endotoxin in the plasma was evaluated with a test box. Gene expression of TNF-α mRNA was assayed using situ hybridization. The area density and the optical density of positive staining expressing TNF-α mRNA were analyzed for the relative content of TNF-α mRNA using situ hybridization and the CMIA medical imaging analysis system. Results There was endotoxemia administration after acute cerebral hemorrhage. It started to increase at 8h after hemorrhage and peaked at 24~36h, and still maintained a high level at 72 h. Expression of TNF-α mRNA in lung, liver, intestines and kidney tissues started to increase at 8h in the model groups and reached a peak at 24~36h. Compared with the normal control and sham-operative groups, expression of TNF-α mRNA was significantly higher at 12~48h in the model groups (P＜0.01). Relative analysis indicated that there was significant positive correlation between the TNF-α mRNA expression in lung, liver, kidney, intestine and plasma endotoxin level (P＜0.01). Conclusion Endotoxemia occurs after cerebral hemorrhage and gene expression of TNF-α increases, which implies that endotoxemia irritates the release of the inflammatory factor, and systemic inflammatory response syndrome (SIRS) develops. This is the key process in generation of CMODS.