中国医师杂志
中國醫師雜誌
중국의사잡지
JOURNAL OF CHINESE PHYSICIAN
2010年
6期
732-735
,共4页
赵伟%张廷威%王瑞琳%张宝生%张宏
趙偉%張廷威%王瑞琳%張寶生%張宏
조위%장정위%왕서림%장보생%장굉
糖尿病,实验性/代谢%糖基化终产物,高级/代谢%肺表面活性物质相关蛋白质A/代谢
糖尿病,實驗性/代謝%糖基化終產物,高級/代謝%肺錶麵活性物質相關蛋白質A/代謝
당뇨병,실험성/대사%당기화종산물,고급/대사%폐표면활성물질상관단백질A/대사
Diabetes mellitus,experimental/ME%Glycosylation end products,advanced/ME%Pulmonary surfactant-associated protein A/ME
目的 探讨实验性糖尿病(diabetes mellitus,DM)大鼠肺组织晚期糖基化终末产物(advanced glycosylated endproducts,AGEs)、肺表面活性物质蛋白质A(surfactant proteins A,SP-A)的变化.方法 48只SD雄性大鼠随机分为DM组和对照组,每组24只.链脲佐菌素(streptozotocin,STZ)60mg/kg尾静脉注射制造DM模型.分别于造模成功后4、12、20周末杀检.免疫组织化学方法 观察肺组织AGEs、SP-A的变化,并进行图像分析(灰度值以0为黑,最大值为白).结果 (1)AGEs:DM大鼠肺泡上皮细胞、支气管黏膜上皮细胞、血管内皮细胞及平滑肌细胞可见大量AGEs阳性细胞,平均灰度值低于对照组(4周93.92±7.92 vs 104.75±8.20;12周76.25±6.76 vs 93.50±7.56;20周47.63±7.96 vs 142.38±19.76;P均＜0.05),随着DM病程的增加逐渐降低.(2)SP-A:4周DM大鼠肺泡Ⅱ型细胞、肺泡巨噬细胞、克拉拉细胞可见少量阳性细胞,12、20周可见大量SP-A阳性细胞,平均灰度值均低于对照组(12周75.63±6.70 vs 110.50±13.20;20周47.38±4.84 vs 97.25±9.87;P均＜0.01).结论 DM大鼠随着病程的增加,出现肺泡Ⅱ型细胞的损伤,可能与AGEs的沉积有关.
目的 探討實驗性糖尿病(diabetes mellitus,DM)大鼠肺組織晚期糖基化終末產物(advanced glycosylated endproducts,AGEs)、肺錶麵活性物質蛋白質A(surfactant proteins A,SP-A)的變化.方法 48隻SD雄性大鼠隨機分為DM組和對照組,每組24隻.鏈脲佐菌素(streptozotocin,STZ)60mg/kg尾靜脈註射製造DM模型.分彆于造模成功後4、12、20週末殺檢.免疫組織化學方法 觀察肺組織AGEs、SP-A的變化,併進行圖像分析(灰度值以0為黑,最大值為白).結果 (1)AGEs:DM大鼠肺泡上皮細胞、支氣管黏膜上皮細胞、血管內皮細胞及平滑肌細胞可見大量AGEs暘性細胞,平均灰度值低于對照組(4週93.92±7.92 vs 104.75±8.20;12週76.25±6.76 vs 93.50±7.56;20週47.63±7.96 vs 142.38±19.76;P均＜0.05),隨著DM病程的增加逐漸降低.(2)SP-A:4週DM大鼠肺泡Ⅱ型細胞、肺泡巨噬細胞、剋拉拉細胞可見少量暘性細胞,12、20週可見大量SP-A暘性細胞,平均灰度值均低于對照組(12週75.63±6.70 vs 110.50±13.20;20週47.38±4.84 vs 97.25±9.87;P均＜0.01).結論 DM大鼠隨著病程的增加,齣現肺泡Ⅱ型細胞的損傷,可能與AGEs的沉積有關.
목적 탐토실험성당뇨병(diabetes mellitus,DM)대서폐조직만기당기화종말산물(advanced glycosylated endproducts,AGEs)、폐표면활성물질단백질A(surfactant proteins A,SP-A)적변화.방법 48지SD웅성대서수궤분위DM조화대조조,매조24지.련뇨좌균소(streptozotocin,STZ)60mg/kg미정맥주사제조DM모형.분별우조모성공후4、12、20주말살검.면역조직화학방법 관찰폐조직AGEs、SP-A적변화,병진행도상분석(회도치이0위흑,최대치위백).결과 (1)AGEs:DM대서폐포상피세포、지기관점막상피세포、혈관내피세포급평활기세포가견대량AGEs양성세포,평균회도치저우대조조(4주93.92±7.92 vs 104.75±8.20;12주76.25±6.76 vs 93.50±7.56;20주47.63±7.96 vs 142.38±19.76;P균＜0.05),수착DM병정적증가축점강저.(2)SP-A:4주DM대서폐포Ⅱ형세포、폐포거서세포、극랍랍세포가견소량양성세포,12、20주가견대량SP-A양성세포,평균회도치균저우대조조(12주75.63±6.70 vs 110.50±13.20;20주47.38±4.84 vs 97.25±9.87;P균＜0.01).결론 DM대서수착병정적증가,출현폐포Ⅱ형세포적손상,가능여AGEs적침적유관.
Objective To approach the changes of advanced glycosylated end products (AGEs),surfactant proteins A (SP-A) in the lung of experimental diabetic rats and their relationship. Methods 48 male SD rats were divided into diabetes mellitus (DM) group and control group, each group with 24 rats.The DM rat model was made by injecting streptozocin (60mg/kg) into caudal vein. The rats were killed and the lung was individually taken out at the end of 4, 12 and 20 weeks after the models were established. The changes of AGEs, SP-A in rats lung were observed with immunohistochemical assay and the images were analyzed( black is minimum of gray, white is maximum of gray ). Results We observed a great quantity of AGEs positive cells in the alveolar epithelial cells, bronchial mucosal epithelium, angio-endothelial cell and smooth muscle cells of the DM rats. The average gray (AG) was inferior to that of the controls(4weeks 93.92 ± 7.92 vs 104. 75 ± 8. 20; 12 weeks 76. 25 ± 6. 76 vs 93.50 ± 7.56; 20 weeks 47.63 ± 7.96 vs 142. 38 ± 19. 76; P ＜0. 05) and decreased with the DM course. In the 4 weeks DM rats, there were a few SP-A positive cells in the type Ⅱ alveolar epithelial cells, Clara cells and alveolar macrophage cells. In the 12 and 20 weeks DM rats, there were a great many CTGF and TGF-β1 positive cells. The AG was inferior to that of the controls( 12 weeks 75.63 ± 6. 70 vs 110. 50 ± 13.20;20 weeks 47.38 ± 4. 84 vs 97. 25 ± 9. 87; P ＜ 0. 01 ). Conclusion With the progress of diabetes, DM rats' pulmonary alveolar type Ⅱ cells injury appeared, that might be related with the deposition of AGEs.
