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目的:研究盲肠结扎穿刺(CLP)诱导的脓毒症大鼠小肠上皮自噬水平,探讨自噬与脓毒症肠上皮损害的关系。方法:建立大鼠盲肠结扎穿刺模型,收集大鼠血清和小肠上皮黏膜,采用酶联免疫吸附法检测血清和黏膜细胞因子的变化,用蛋白免疫印迹法和rt-PCR法检测小肠黏膜组织中自噬相关蛋白的表达量以及转录水平,对获取的数据进行统计学处理。结果:CLP诱导的脓毒症大鼠血清和黏膜细胞因子TNF-α在4 h即明显升高,与对照组比有显著性差异(P<0.05)。自噬相关蛋白LC3-Ⅱ/LC3在脓毒症8 h明显升高,12 h下降,与对照组比有显著性差异(P<0.05)。LC3基因也表现出早期升高随之下降的趋势。结论:大鼠在脓毒症时,小肠黏膜受损,其自噬相关蛋白表达早期升高,随后下降。自噬受细胞因子水平的影响,导致肠黏膜上皮细胞功能失调。
Objective: To study the intestinal autophagy in septic rats induced by cecal ligation and puncture (CLP) and to explore the relationship between autophagy and intestinal epithelial damage in sepsis. Methods: The cecal ligation puncture model was established in rats. Serum and intestinal epithelial mucosa were collected and the changes of serum and mucosal cytokines were detected by enzyme-linked immunosorbent assay (ELISA). The protein expressions of Related protein expression levels and transcription levels, the data obtained for statistical analysis. Results: The serum and mucosal cytokine TNF-α in CLP-induced sepsis rats increased significantly at 4 h, which was significantly different from that of the control group (P <0.05). LC3-Ⅱ / LC3, an autophagy-related protein, was significantly increased at 8 h after sepsis and decreased at 12 h, which was significantly different from the control group (P <0.05). The LC3 gene also showed a tendency to decrease in the early stage. Conclusion: In sepsis, small intestinal mucosa is impaired and the expression of autophagy-related protein is increased early and then decreased. Autophagy is affected by cytokine levels, resulting in dysfunctional intestinal epithelial cells.