首页> 中文期刊>脑与神经疾病杂志 >核转录因子-κB 在糖尿病大鼠穹窿下器细胞的表达

核转录因子-κB 在糖尿病大鼠穹窿下器细胞的表达

     

摘要

目的:观察核转录因子-κB ( NF-κB)在不同时期糖尿病大鼠穹窿下器( SFO)中的表达并探讨其表达的意义。方法雄性Wistar大鼠,模型组每只大鼠给予链脲佐菌素60mg· kg-1,腹腔一次性注射,建立1型糖尿病大鼠模型。用免疫组织化学染色方法观察NF-κB在正常大鼠及2、4、8 w糖尿病大鼠SFO细胞内的表达。结果对照组NF-κB免疫阳性细胞稀少,胞核呈浅棕黄色,平均吸光度为156.42±7.25。2w组NF-κB免疫强阳性细胞SFO内均匀分布,核呈棕褐色,高度表达,为强阳性,平均吸光度为183.72±8.35。4w组SFO NF-κB的表达水平有所下降但仍高于正常对照组,平均吸光度为169.55±5.84。8w组NF-κB免疫强阳性细胞的表达与正常对照组无明显区别,平均吸光度为158.32±8.72。平均吸光度测定:2w组>4w组>8w组, P ﹤0.05,8w组与对照组比较P﹥0.05。结论 NF-κB在糖尿病大鼠SFO细胞内呈短暂一过性的表达增强,NF-κB途经可能在糖尿病大鼠 SFO细胞损伤中起着重要的作用。%Objective To observe the expression of changes of nuclear transcription factor kappa B ( NF-κB) in subfornical organ ( SFO) in different stages of diabetic rat .Methods Male Wistar rats , each rat of model group was given streptozotocin ( STZ) 60mg · kg-1 by intraperitoneal injection all at once to establish type 1 diabetic rat model .Immunohistochemical staining was used to observe the expression of NF-κB in subfornical organ of normal rats and diabetic rats in 2,4,8,12 weeks.Results Numbers of immunopositive cells of NF-κB were scarce, nuclei were light brown yellow,and the average optical density was 156.42±7.25.2 weeks group, NF-κB-positive cells in SFO were evenly distributed , highly expressed, nuclei were brown, and the average optical density was 183.72±8.35.4 weeks group , the expression level of NF-κB positive cells in SFO was decreased but still higher than the normal control group, the average optical density was .There was no significant difference between 8 weeks group and normal control group in the expression of NF-κB strongly positive cells , the average optical density was 158.32 ±8.72. Average optical density measurement results:2 weeks group>4 weeks>8 weeks group , with statistical significance (P<0.05), 8 weeks group and the control group had no significant difference ( P>0.05).Conclusion Among different diabetic rat models of different times , NF-κB expression in the SFO is transient enhanced , which indicates that NF-κB pathway may play an important role in damage of SFO in diabetic rats .

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