Somfai Gábor Márk, Knippel Barbara, Ruzicska Eva, Stadler Krisztián, Tóth Miklós, Salacz György, Magyar Kálmán, Somogyi Anikó
Faculty of Medicine, 2nd Department of Ophthalmology, Semmelweis University, Mária str. 39, H-1085 Budapest, Hungary.
Neurochem Int. 2006 Jun;48(8):746-52. doi: 10.1016/j.neuint.2005.12.009. Epub 2006 Mar 9.
Diabetes is known to increase the risk of Alzheimer's disease (AD) and vascular dementia via oxidative stress and inflammation. There are speculations that SSAO activity might be related to the development of AD. Our aim was to investigate whether changes of soluble SSAO activity, oxidative stress and inflammation markers are related to each other in diabetes. Soluble and tissue-bound SSAO activities (from serum and aorta, respectively) were determined in streptozotocin (STZ)-induced diabetic rats without insulin treatment, receiving insulin once, or twice daily compared to control animals. After three weeks of treatment soluble and tissue-bound SSAO activities (seSSAO and aoSSAO, respectively), serum total antioxidant status (TAS), high sensitivity C-reactive protein (hsCRP), fructose amine levels and routine laboratory parameters were determined. SeSSAO activity significantly increased in the diabetic groups without treatment and receiving insulin once daily, and a marked decrease in aoSSAO activity was seen in all diabetic groups. Increased oxidative stress was correlated with hsCRP elevation, while hsCRP and seSSAO activity were also significantly correlated. In all groups seSSAO and aoSSAO activities were in negative correlation with each other. Our results support the view that poor metabolic control leads to increased oxidative stress, which in turn may cause the elevation of hsCRP levels. Soluble SSAO on the one hand acts as an adhesion molecule--thus possibly being a factor responsible for the late complications of diabetes--and on the other hand, it may contribute to oxidative stress. Our parsimonious conclusion is that there is a relation between the risk factors of AD and vascular dementia (diabetes, oxidative stress and chronic inflammation) and SSAO activity, which may originate from the vessel wall.
众所周知，糖尿病会通过氧化应激和炎症增加患阿尔茨海默病（AD）和血管性痴呆的风险。有人推测，SSAO活性可能与AD的发展有关。我们的目的是研究糖尿病患者中可溶性SSAO活性、氧化应激和炎症标志物的变化是否相互关联。与对照动物相比，在未接受胰岛素治疗、每日接受一次胰岛素或每日接受两次胰岛素治疗的链脲佐菌素（STZ）诱导的糖尿病大鼠中，分别测定了可溶性和组织结合性SSAO活性（分别来自血清和主动脉）。治疗三周后，测定了可溶性和组织结合性SSAO活性（分别为seSSAO和aoSSAO）、血清总抗氧化状态（TAS）、高敏C反应蛋白（hsCRP）、果糖胺水平和常规实验室参数。未经治疗和每日接受一次胰岛素治疗的糖尿病组中seSSAO活性显著增加，所有糖尿病组中aoSSAO活性均显著降低。氧化应激增加与hsCRP升高相关，而hsCRP与seSSAO活性也显著相关。在所有组中，seSSAO和aoSSAO活性彼此呈负相关。我们的结果支持这样一种观点，即代谢控制不佳会导致氧化应激增加，进而可能导致hsCRP水平升高。一方面，可溶性SSAO作为一种粘附分子——因此可能是糖尿病晚期并发症的一个因素——另一方面，它可能导致氧化应激。我们的简要结论是，AD和血管性痴呆的危险因素（糖尿病、氧化应激和慢性炎症）与SSAO活性之间存在关联，这可能源于血管壁。
