慢性间歇性低氧激活内质网应激介导大鼠肾脏损伤

发布时间：2018-05-23 16:36

本文选题：阻塞性睡眠呼吸暂停低通气综合征 + 慢性间歇性低氧　；参考：《中国呼吸与危重监护杂志》2017年04期

【摘要】：目的探讨慢性间歇性低氧在普通饮食及高脂饮食引起肾脏损伤中的作用机制。方法将SPF级健康雄性Wistar大鼠24只,随机分为4组(每组6只),分别为A组(常氧并普通饮食)、B组(常氧并高脂饮食)、C组(慢性间歇性低氧并普通饮食)和D组(慢性间歇性低氧并高脂饮食)。6周后检测血清中肾脏早期损伤指标半胱氨酸蛋白酶抑制剂C(Cys-C),行肾脏CHOP蛋白免疫组化,并在电镜下观察肾小球及肾小管超微结构变化。结果 B组、C组、D组中肾早损指标Cys-C水平较A组显著升高,且在D组中值最高(均P0.05);B组、C组、D组中内质网应激标志性蛋白CHOP平均光密度值与A组比较显著升高,且在D组中值最高(均P0.05)。电镜下观察,A组肾小球及肾小管未见明显异常;B组、C组近曲肾小管上皮细胞局灶性核固缩,刷状缘稀疏并脱落;D组中有大片肾小管上皮细胞核固缩,刷状缘稀疏并脱落。结论慢性间歇性低氧、高脂饮食可通过激活内质网应激介导近曲肾小管上皮的凋亡,使肾脏的超微结构发生改变,进而导致肾脏功能损伤。
[Abstract]:Objective to investigate the mechanism of chronic intermittent hypoxia on renal injury induced by common diet and high fat diet. Methods 24 SPF healthy male Wistar rats were used. They were randomly divided into 4 groups (6 rats in each group): group A (normoxic plus general diet) group B (normoxic and hyperlipidemic diet group C) and group D (chronic intermittent hypoxia with hyperlipidemia diet) and group D (chronic intermittent hypoxia combined with hyperlipidemia diet for 6 weeks). The early damage index of kidney was detected, and the cysteine protease inhibitor, Con Cys-Cn, was used to detect the renal CHOP protein immunohistochemistry. The ultrastructural changes of glomeruli and renal tubules were observed under electron microscope. Results the Cys-C level of early renal damage in group B was significantly higher than that in group A, and the median value was the highest in group D (P 0.05). The mean optical density of CHOP in group D was significantly higher than that in group A. The median value was the highest in group D (P 0.05). There were no obvious abnormalities in glomeruli and tubules in group A and tubules. In group C, focal nuclear contraction of proximal tubule epithelial cells was observed. In group D, a large number of renal tubule epithelial nuclei were condensed and abscission, while the brush edges were sparse and abscission. Conclusion chronic intermittent hypoxia and high fat diet can induce apoptosis of proximal tubule epithelium through activation of endoplasmic reticulum stress.
【作者单位】：兰州大学第一临床医学院;兰州大学第一医院呼吸科;
【基金】：甘肃省自然科学基金(1506RJZA254)
【分类号】：R692;R766

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