高糖及高胰岛素对肺泡巨噬细胞吞噬功能和超微结构的影响

Effect of high glucose or high glucose and high insulin level on phagocytotic function and ultrastructure of activated rat alveolar macrophages

目的和方法：选用正常大鼠肺泡巨噬细胞（ＡＭ），在高糖及高糖＋高胰岛素环境下培养，用卡介苗（ＢＣＧ）、干扰素ａ－２ｂ（ＩＦＮα－２ｂ）或两者联合活化，检测其贴壁率、四唑氮兰（ＮＢＴ）还原功能、ＮＯ和ＴＮＦ－α释放量并观察其超微结构改变。结果：高糖及高糖＋高胰岛素环境下活化ＡＭ贴壁延迟（Ｐ＜０．０１），ＮＢＴ还原功能明显被抑制（Ｐ＜０．０１）；ＢＣＧ和ＩＦＮα－２ｂ＋ＢＣＧ活化ＡＭ时，其ＮＯ和ＴＮＦα释放量均明显低于对照组（Ｐ＜０．０１）；ＩＦＮα－２ｂ活化ＡＭ时，其ＮＯ和ＴＮＦ－α释放量与对照组无明显差别（Ｐ＞０．０５）；细胞表面伪足减少、变短，胞质内高尔基氏体、粗面内质网减少。结论：在短期内高糖及高糖＋高胰岛素环境均抑制ＡＭ吞噬功能及改变超微结构，从而使糖尿病个体易发生肺部感染。

AIM: The phagocytotic function and morphological changes of pulmonary alveolar macrophages (AM) of rat in high glucose or high glucose and high insulin conditions were studied. METHODS: AM were harvested from Wistar rats by bronchoalveolar lavage and were activated by Bacille Calmette - Guerin (BCG), interferon a - 2b (IFNa - 2b)or BCG and IFNa - 2b. The adherent rate, nitroblue retrazolium (NBT). reduction function and the concentrations of NO and TNF-a in culture rat AM were evaluated. The ultrastructure of AM was Observed by using transmission elects microscopy and scanning electron microscopy. RESULTS: In high glucose or high glucose glucose and high insulin conditions, the adherence of AM postponed(P＜ 0.01 ), NBT reduction of AM significantly decreased(P＜0.01); the volume of NO and TNF-a produced by AM after stimulation with BCG and IFNa-2b + BCG was significantly lower in high glucose groups than in the controls (P ＜ 0.01); their surface pseudopodia was reduced and shortened and the numbers of Golgi apparatus and rough endoplasmic reticulum decreased. CONCLUSIONS:The impaired phagocytotic function and ultrastructure of activated rat AM were much the same regardless of high glucose or high glucose and high insulin level in a short time. Diabetic subjects were predisposed to infection of the lung, which was frequently recurrent or even fatal.