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高脂血症大鼠肾脏一氧化氮变化及其意义
The Change of Nitric Oxide in Hypercholesterilemia rats and Its effect on Lipid renal Damage
【摘要】 为探讨高脂饲料对大鼠肾脏的损害及其一氧化氮的变化,用含4%胆固醇及1%胆酸钠的饲料饲喂大鼠建立高脂模型,观察大鼠尿蛋白排泄量,测定血清脂质及肾皮质、尿一氧化氮含量,并测肾组织诱生型一氧化氮合酶的表达及肾组织中细胞凋亡情况。结果显示8周后大鼠肾皮质及尿中一氧化氮含量增多,24h尿蛋白排泄增加,肾小管诱生型一氧化氮合酶表达增强,其表达强度与肾组织中细胞凋亡数量正相关。揭示在高脂饮食导致的肾损害中诱生型一氧化氮合酶可能通过诱导细胞凋亡参与肾小管间质损害
【Abstract】 In order to investigate the role of nitric oxide (NO) in renal damage by lipid, the NO contents in cortex renis and urine in rats supplementded with 4 % cholesterol and 1 % cholic acid for 8 weeks were measured and the NO - x was determined by the expression of a measure of NO content. The expression of inducible nitric oxide synthase (iNOS) on kidney tissue was studied by using immunohistochemistry methods. The apoptosis cells in the glomeruli, tubules and interstitium in the animals of two groups were identified by in situ nick end labeling of fragmented DNA with terminal deoxynucleotidyl transferase and biotinylated deoxyuridine. Cortex renis NO content in hypercholesterolemia rats (CHR) was higher than in normal rats(NR) ( P <0.05). The NO - X production in 24 h urine in CHR was increased as compared with that in NR ( P <0.01), and iNOS expression in CHR was stronger than in NR. The index of TdT positive cells within glomeruli and tubules in CHR was higher than in NR ( P <0.01 for both). The iNOS expression was significantly correlated with TdT positive cell index in CHR group ( P <0.01). The NO product in cortex renis was correlated with 24 h urine protein in CHR ( r =0.51, P <0.05). It was concluded that expression of iNOS caused the NO increase in CHR. NO might play an important role in renal tubulointerstitium injury by cell apoptosis.
【Key words】 hypercholesterolemia; nitric oxide; inducible NO synthase; apoptosis;
- 【文献出处】 同济医科大学学报 ,ACTA UNIVERSITATIS MEDICTNAE TANGJI , 编辑部邮箱 ,1999年02期
- 【被引频次】11
- 【下载频次】67