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目的该实验旨在研究急性肺损伤(ALI)时肺泡Ⅱ型上皮细胞(AEC-Ⅱ)超微结构变化和肺组织表面活性蛋白SP-A含量的变化关系,从而探讨ALI的发病机制。方法48只Sprague-Dawley幼鼠被随机分为正常对照组和ALI组。腹腔注射脂多糖(LPS,4 mg/kg)建立ALI模型,正常对照组注射等量生理盐水。LPS注射后24,48,72 h每亚组各处死8只大鼠。取左肺下肺组织待透射电镜检查。用Western blot方法测定肺组织SP-A的相对含量。结果ALI 24 h时,AEC-Ⅱ微绒毛消失。24 h及48 h时板层小体(lamellar body,Lb)数量增加,体积增大,密度减低,排空明显增强,呈指环状绕核排列,细胞增生活跃,代谢旺盛。48 h时Lb呈巨大空泡样变性。肺组织SP-A含量明显高于对照组(24 h时ALI组为6.52±0.62,对照组为5.02±0.35,P<0.01;48 h时ALI组为6.65±0.62,对照组为5.01±0.36,P<0.01)。72 h时Lb破溃,数目明显减少,细胞核形态不规则,部分核边界不清,肺组织SP-A含量下降(ALI组为3.87±0.50,对照组为5.22±0.36,P<0.01)。结论LPS致幼鼠ALI时AEC-Ⅱ和肺组织SP-A的变化为时间依赖性,随AEC-Ⅱ损伤程度的加重肺组织SP-A由代偿转为失代偿,可能是发生ARDS的重要机制之一。
Objective To study the relationship between ultrastructural changes of alveolar type Ⅱ epithelial cells (AEC-Ⅱ) and the content of SP-A in lung tissue during acute lung injury (ALI), and to explore the pathogenesis of ALI. Methods 48 Sprague-Dawley rats were randomly divided into normal control group and ALI group. The model of ALI was established by intraperitoneal injection of lipopolysaccharide (LPS, 4 mg / kg), and the normal control group was injected with the same amount of saline. Eight rats were sacrificed in each subgroup 24, 48 and 72 h after LPS injection. Take the left lung tissue to be examined by transmission electron microscopy. Western blot was used to determine the relative content of SP-A in lung tissue. Results ALI 24 h, AEC-Ⅱ microvilli disappeared. At 24 h and 48 h, the lamellar body (Lb) increased in number, increased in volume, decreased in density and evacuated significantly, showing a ring-like arrangement of nuclei around the nucleus, with active cell proliferation and strong metabolism. Lb was a huge vacuolar degeneration at 48 h. The content of SP-A in lung tissue was significantly higher than that in the control group (6.52 ± 0.62 in ALI group and 5.02 ± 0.35 in control group at 24 h, P <0.01; 6.65 ± 0.62 in ALI group and 5.01 ± 0.36 in control group at 48 h, P <0.01). The number of Lb was significantly reduced at 72 h. The morphology of nucleus was irregular. Some nuclear boundaries were unclear. The content of SP-A in lung tissue was decreased (3.87 ± 0.50 in ALI group and 5.22 ± 0.36 in control group, P <0.01). Conclusions The changes of AEC-Ⅱ and SP-A in lung tissue of LPS-induced acute lung injury in a time-dependent manner. With the severity of AEC-Ⅱ injury, SP-A in lung tissue is decompensated to decompensation, which may be ARDS One of the important mechanisms.