大鼠脑缺血再灌注后糖基化终产物及其受体RAGE、分泌型RAGE的表达被引量：3

The expression of advanced glycation end-products,its receptor and soluble RAGE in rats with focal cerebral ischemia-reperfusion

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摘要目的:探讨大鼠脑缺血再灌注后血清分泌型RAGE、缺血脑组织糖基化终产物及其受体RAGE的表达。方法:本实验分为假手术组和脑缺血2 h后再灌注12 h、24 h、48 h组,共四个实验组,每组20只健康成年大鼠,雌雄不限。应用单侧大脑中动脉阻断法制作局灶型脑缺血模型,脑缺血2 h后再灌注。采用ELISA法检测血清分泌型RAGE水平,免疫组化法检测缺血脑组织糖基化终产物及其受体的变化,应用原位杂交法检测RAGEm-RNA。结果:与假手术组比较,脑缺血再灌注后大鼠血清分泌型RAGE水平下降。免疫组化结果显示脑组织糖基化终产物及其受体蛋白表达的阳性细胞数量与假手术组比较,呈增高趋势,再灌注24 h时,糖基化终产物及其受体蛋白表达达高峰,再灌注48 h时,表达有所下降。统计学分析提示再灌注24 h组、48 h组分别与假手术组比较,差异显著,具有统计学意义(P<0.05-0.01),而两组之间相比较,无显著差异(P>0.05)。原位杂交法检测脑缺血再灌注48 h组缺血脑组织RAGEmRNA阳性细胞数增加,与假手术组比较,差异具有统计学意义(P<0.01)。结论:脑缺血再灌注后缺血脑组织糖基化终产物及其受体的表达升高,而分泌型RAGE在大鼠脑缺血再灌注后血清中的含量及脑组织内的表达均下降。上述变化可能是脑缺血再灌注损伤的机制之一。 Objective： to explore the expression of advanced glycation end-products, its receptor and soluble RAGE in rats with focal cerebral ischemia/reperfusion （I/R）. Methods： Forty SD rats were divided into sham-operated group （Sham group）, ischemia for 2 h and reperfusion for 12 h group（I/R 12 h group） ,24 h group （I/R 24 h group） and 48 h group （ I/R 4 8h group）. The focal cerebral ischemia and reperfusion model was induced by ligation with nylon monofil- ament in rats. The expression of AGEs, RAGE in the cortex of ischemic hemisphere was determined by immunohisto- chemistry. In situ hybridization was performed to examine the expression of RAGEmRNA. Serum sRAGE were measured by ELISA method. Results： A small amount of AGEs, RAGE -positive cells were observed in the sham-operated group, while the number of AGEs, RAGE -positive cells increased in the cortex of ischemic hemisphere. They were significantly more in I/R 24 h group than those in the sham-operated group （P 〈0.05-0.01 ）. Expressions of AGEs and RAGE rise to the peak at I/R 24 h, and then began to descend gradually, while RAGE mRNA expression was present in a lower level in the sham-operated group, the number of RAGE mRNA positive neuron increased in the ischemia-reperfusion group.There was significant difference between the sham-operated group and I/R 24 h group in the expression of RAGEmRNA. Serum sRAGE were greatly decreased in the ischemia-reperfusion group in contrast to the sham-operated group （P 〈 0.01 ）. Conclusion： The axis of AGEs -RAGE is probably the therapic target of cerebral ischemia reperfusion injury.

作者么晓轶李颖

机构地区哈尔滨医科大学附属第二临床医院干部三病房

出处《神经解剖学杂志》 CAS CSCD 北大核心 2013年第4期399-404,共6页 Chinese Journal of Neuroanatomy

基金黑龙江省教育厅科学技术研究项目(11531215)

关键词脑缺血糖基化终产物 RAGE AGEs RAGE sRAGE focal cerebral ischemia/reperfusion （I/R）

分类号 R743 [医药卫生—神经病学与精神病学]

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1Longa EZ, Weinstein PR, Carlson S, et al. Reversible middle cere- bral artery occlusion without craniectomy in rats [ J ]. Stroke, 1989, 20:84 -91.
2Bodiga VL, Eda SR, Bodiga S. Advanced glycation end products: role in pathology of diabetic cardiomyopathy [ J ]. Heart Fail Rev, 2013, 13:28-34.
3Wei Q, Ren X, Jiang Y, et al. Advanced glycation end products ac- celerate rat vascular calcification through RAGE/oxidative stress [J]. BMC Cardiovasc Disord, 2013, 13:13.
4Gkogkolou P, Bfihm M. Advanced glycation end products: key play- ers in skin aging? [J]. Dermatoendocrinol, 2012, 4:259 -270.
5Busch M, Franke S, Rtister C, et o2. Advanced glycation end-prod- ucts and the kidney[J]. Eur J Clin Invest, 2010, 40:742 -755.
6Liu Y, Ma Y,Wang R, et al. Advanced glycation end products ac- celerate ischemia/reperfusion injury through receptor of advanced end product/nitrative thioredoxin inactivation in cardiac microvascu- lar endothelial cells[ J ]. Antioxid Redox Signal, 2011, 115 : 1769 - 1778.
7Kamide T, Kitan Y, Takeichi T, et al. RAGE mediates vascular in- jury and inflammation after globalcerebral ischemia[ J]. Neurochem Int, 2012, 60:220-228.
8Ohnuki Y, Nagann R, Takizawa S, et al. Advanced glycation end products in patients with cerebral infarction[ J]. Intern Med, 2009, 48:587 - 589.
9Li J, Liu D, Sun L, et al. Advanced glyeation end products and neu- rodegenerative diseases: mechanisms and perspective[ J]. J Neurol Sci, 2012, 317:1 -5.
10Kanauchi M, Tsujimoto N, Hashimoto T. Advanced glycation end products in Nondiabetic patients with coronary artery disease [ J ]. Diabetes Care, 2001, 24:1620 - 1623.