摘要
目的:研究慢性应激对正常及糖尿病倾向小鼠各组织抗氧化酶影响的差异并探讨其意义。方法:用链脲佐菌素(STZ)复制糖尿病倾向小鼠模型(STZ鼠),予以6周慢性多相性应激(限制、旋转、拥挤),检测其空腹血糖(FBG)、空腹胰岛素(FINS)水平和胰、心、肝组织超氧化物歧化酶(SOD)、谷肽甘肽过氧化物酶(GSH-PX)活性及脂质过氧化物(LPO)含量。结果:慢性应激使STZ鼠FBG水平升高,FINS水平未增高;对STZ鼠各组织抗氧化酶活性有不同影响:加重其胰腺SOD活性下降和LPO含量升高,并使其GSH-PX活性降低(P均<0.05),对其肝脏显示使SOD、GSH-PX活性升高和LPO含量下降的相反作用(P均<0.05)。结论:慢性应激及STZ诱导的糖尿病倾向协同作用特异地加重小鼠胰腺抗氧化酶活性下降和脂质过氧化物形成,可能参与损害其胰岛素分泌功能和导致高血糖症。
To investigate the degree of difference and direction of alterations of antioxidant enzyme activities in different tissues of normal and diabetes-prone animals by chronic stress and to explore its implications. Methods: The levels of fasting blood glucose (FBG) and fast plasma insulin (FINS), the activities of superoxide dismutase (SOD) and glutathione peroxidase (GSH-PX) and level of lipid peroxidate (LPO) were measured in the pancreas, heart and liver of normal and streptozotocin-induced diabetes-prone mice (STZ mice) exposed to multiple stressors (restrain, rotation, crowding) for 6 weeks. Results: The FBG level in STZ mice was elevated by stress, while the FINS level was not increased. In the pancreas of STZ mice, SOD activity was decreased and LPO formation increased ( P <0.05); these negative changes resulting from STZ were exacerbated by chronic stress ( P <0.05). However, opposite changes occurred in the liver of STZ mice after chronic stress (increased in SOD and GSH-PX activities, decreased in LPO content, P <0.05). On the other hand, chronic stress resulted in less change in normal mice (increased in SOD activity in heart, P <0.05). Conclusion: The synergistic actions of chronic stress and STZ-induced diabetes-prone status can exacerbate the decrease of antioxidant enzyme activities and formation of LPO in the pancreas of mice specifically. This may impair insulin secretion and promote heperglycemia in STZ mice.
出处
《中国临床心理学杂志》
CSCD
2000年第1期19-22,共4页
Chinese Journal of Clinical Psychology
基金
国家自然科学基金!资助重点项目(项目号 :3 94 3 0 0 70 )
关键词
慢性应激
糖尿病
胰岛素
抗氧化酶
LPO
Chronic stress, Diabetes mellitus, Insulin, Antioxidant enzymes, Lipid peroxidation
