论文部分内容阅读
目的从细胞受体和免疫分子水平探讨T2DM内毒素性肺损伤肺局部防御功能减弱的机制。方法雄性Wistar大鼠高糖高脂饲料喂养,小剂量链脲佐菌素(STZ)注射建立T2DM大鼠模型。经尾静脉注射脂多糖(LPS)建立内毒素血症/急性肺损伤大鼠模型。肺泡巨噬细胞(AM)表面CD14表达测定采用免疫组化法,并进行计算机图像分析。放免法检测血清及肺组织匀浆液中TNF-α、IL-6的水平。结果T2DM大鼠AM表面CD14表达和血清TNFα-、IL-6水平明显高于正常对照大鼠(P<0.05)。而经LPS激活后,T2DM及正常对照大鼠AM表面CD14表达及血清、肺组织匀浆液中TNF-α、IL-6水平明显增高(P<0.05),但T2DM组上述指标低于正常对照组,差异有统计学意义(P<0.01)。结论T2DM肺组织的局部防御功能减弱可能与AM经LPS激活后CD14分子上调表达减弱及分泌TNF-α、IL-6能力下降有关。
OBJECTIVE: To investigate the mechanism of diminished local defensive function of lung in T2DM endotoxin-induced lung injury from the level of cellular receptors and immune molecules. Methods Male Wistar rats were fed with high-sucrose and high-fat diet and low-dose streptozotocin (STZ) injection to establish T2DM rat model. The rat model of endotoxemia / acute lung injury was established by injecting lipopolysaccharide (LPS) through tail vein. CD14 expression on alveolar macrophages (AM) was detected by immunohistochemistry and analyzed by computer image. The levels of TNF-α and IL-6 in serum and lung homogenate were detected by radioimmunoassay. Results The expression of CD14 on AM and the level of TNFα- and IL-6 in T2DM rats were significantly higher than those in normal control rats (P <0.05). However, after activated by LPS, the expression of CD14 on AM surface and the level of TNF-α and IL-6 in serum and lung homogenate significantly increased in T2DM and normal control rats (P <0.05), but the above indexes in T2DM group were lower than those in normal control group , The difference was statistically significant (P <0.01). Conclusion The decreased local defensive function of T2DM lung tissue may be related to the down-regulation of CD14 expression and the decrease of the secretion of TNF-α and IL-6 after AM activation by LPS.