机构地区:[1]中南大学湘雅二医院老年病科,长沙410011
出 处:《中国行为医学科学》2004年第2期121-123,共3页Chinese Journal of Behavioral Medical Science
基 金:国家自然科学基金重点资助项目 (39430 0 70 )
摘 要:目的研究实验性长期心理应激对链脲佐菌素 (STZ)诱导鼠 (STZ鼠 )血糖、胰岛内分泌功能和组织形态学的影响 ,探讨其与氧自由基代谢的关系。方法 2 0只正常昆明小鼠按性别匹配随机分入A组 (正常鼠无应激组 ,10只 )和B组 (正常鼠应激组 ,10只 ) ,40只STZ鼠 (血糖 <13 .9mmol/L)按性别、血糖匹配后随机分入C组 (STZ鼠无应激组 ,2 0只 )和D组 (STZ鼠应激组 ,2 0只 ) ,B、D组给予 6周旋转、限制、拥挤应激刺激 ,A、C组则否。测血糖 (BG)并测定胰岛组织胰岛素 (PI)、胰高糖素 (PG)、脂质过氧化物 (LPO)、总超氧化物歧化酶 (总SOD)、谷胱甘肽过氧化物酶 (GSH Px)和一氧化氮 (NO) ,光镜和电镜观察胰岛组织形态。结果应激后D组血糖 ( 10 .3± 6.2mmol/L)较其他 3组显著增高 ,PI含量显著下降 ,总SOD和GSH Px活性显著降低 ,LPO、NO含量和胰岛炎评分显著增高 (P均 <0 .0 5 ) ;STZ药物与应激刺激对于升高BG、胰腺组织LPO和NO含量以及胰岛炎评分、降低PI和总SOD以及GSH Px活性有协同作用 ( P 均 <0 .0 5 ) ,电镜下显示D组胰岛 β细胞超微结构损伤明显 ,而α细胞损伤相对轻微 ;胰岛炎评分与胰腺组织LPO、NO含量呈中度正相关 (P均 <0 .0 1)。结论实验性长期心理应激可损伤STZ鼠胰岛分泌胰岛素功能 ,并加重胰岛炎 ;局部氧?Objective To investigate the effects of long term psychological stressors on islet histomorphology and endocrine functions of streptozotocin- induced mice (STZ mice), and explore the possible factors that impair islets in STZ mice histomorphology and endocine functions through oxygen free radical mechanism. MethodsTwenty KM mice were matched with sex and divided randomly into Group A (normal mice, no stress) and Group B (normal mice, stress), while forty STZ mice into Group C (STZ mice, no stress) and Group D (STZ mice, stress). Groups B and D were exposed to multiple stressors (restrain, rotation, crowding) for 6 weeks. Before and after the experiment, blood glucose levels(BG) were measured. By the end of the experiment, pancreas samples were collected to determine the concentrations of insulin (PI), glucagon (PG), lipid peroxidate (LPO) and nitric oxide (NO), the activities of total superoxide dismutase (total SOD) and glutathione peroxidase (GSH-Px) in pancreas. The severity of insulitis was graded with light microscope, and the ultramicrostructure of α and β cells in pancreatic islets was observed with electron microscope. ResultsAfter stress, in Group D, the BG level significantly increased and PI concentration decreased, the activities of total SOD and GSH-Px decreased while the contents of LPO and NO increased (P<0.05). More islets showed insulitis in Group D and the average grade of insulitis was higher (P<0.05). The ultrastructure of β cells in islets of Group D was impaired severely while α cells were only injured mildly. There were moderate positive correlation between the grade of insulitis and the contents of LPO and NO in pancreas. Conclusion Long-term experimental psychological stressors can impair pancreatic islets’ secreting insulin in STZ mice and exacerbate its insulits. The dysfunction of oxygen free radical metabolism and overproduction of NO locally might participate in this pathologic process.
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