摘要
目的观察过氧化脂质体增殖激活受体γ(PPARγ)激动剂噻唑烷二酮类化合物(罗格列酮,RGZ)对高糖刺激大鼠肾小球系膜细胞细胞间粘附分子-1(ICAM-1)和β1整合素表达的影响,了解PPARγ与粘附分子的关系。方法体外培养大鼠HBZY-1肾小球系膜细胞,分为9组:正常糖组,高糖组,甘露醇组,正常糖及高糖加1、5、10μm o l/L罗格列酮组。干预作用24 h后采用细胞免疫组化染色检测ICAM-1表达,间接免疫荧光染色及流式细胞仪检测β1整合素表达。结果高糖刺激使系膜细胞ICAM-1、β1整合素表达增加,且不依赖于渗透压。罗格列酮能够抑制正常糖和高糖诱导的系膜细胞ICAM-1、β1整合素表达;高糖组罗格列酮抑制作用更强,且呈剂量依赖性。β1整合素与ICAM-1呈正相关。结论粘附分子参与了糖尿病肾病(DN)发病机制,PPARγ激动剂罗格列酮可能通过对高糖刺激粘附分子表达的抑制效应而影响DN系膜扩张和肾小球硬化过程。
Objective To observe the effects of PPARγ activators thiazolidinediones （Rosiglitazone） on the expression of intercellular adhesion molecule-1 （ICAM-1） and β1 integrin in high glucose-induced rat glomerular mesangial cells （GMC） in order to elucidate the relationship between PPARγ and adhesion molecules. Methods Rat HBZY-1 GMCs were cultured in vitro and divided into 9 groups： Normal Glucose group（N）, High Glucose group（H）, Mannitiol group（M）, Normal and High Glucose plus 1, 5, 10 μmol/L Rosiglltazone. Every group was treated for 24 hours. The expression of ICAM-1 was measured by immunohistochemistry, the expression of β1 integrin by indirect immunofluorescence staining and flow cytometry. Results It was found that high glucose can significantly increase the expression of ICAM-1 and β1 integrin in GMCs, which is independent of the osmotic pressure. Rosiglitazone can inhibit the expression of ICAM-1 and β1 integrin in normal and high glucose treated GMCs, and the inhibition is stronger in high glucose treated-group, which is in a dose-dependent manner. The expression of β1 integrin is positively correlated with ICAM-1. Conclusion Adhesion molecules involves in the pathogenesis of diabetic nephropathy （DN）. PPARγ activators-Rosiglitazone may exert effect on mesangial expansion and glomerulosclerosis in DN through the inhibition of expressions of adhesion molecules induced by high glucose.
出处
《四川大学学报（医学版）》
CAS
CSCD
北大核心
2006年第4期599-601,610,共4页
Journal of Sichuan University(Medical Sciences)
作者简介
Corresponding author,E-mail：hsongm@hotmail.com
