肥大细胞与肾纤维化

肥大细胞是多种介质和细胞因子的产生细胞。它直接或间接参与机体的多种生理和病理过程。近年的研究发现 ,肥大细胞与肾纤维化也有较为密切的关系 ,机制尚不完全清楚。本文就这方面的研究进展作一综述     

CD2相关蛋白在肾脏固有细胞中的表达及分布

CD2相关蛋白（CD2AP）是与蛋白尿发生密切相关的足细胞分子。近年研究表明，CD2AP不仅是足细胞足突间裂孔隔膜的重要成分，而且还参与细胞骨架的重构，可能参与细胞许多重要的生理功能。本研究通过观察CD2AP在。肾脏固有细胞中的分布及其在足细胞分化中的分布变化，初步探讨其在足细胞中的生理功能。     

The Effect of Ligustrazine on Peritoneal Transport in Peritoneal dialysis

In order to investigate the effect of ligustrazine (Lig)i.p.on peritoneal permeability in peritoneal dialysis and its side effects,creatinine was given intravenously and continuously to maintain the high plasma creatinine level.All the rabbits were divided into three groups:normal control group (goup A),group B treated with 0.12% Lig and group C treated with 0.24% Lig.The peritoneal dialysis of all rabbits lasted 2h.The plasma and dialysate levels of glucose,protein and creatining were observed immediate,30min,60min,90min,120min after dialysis.Creastinine dialysate/plasma ratio (D/P),protein D/P ratio,grucose D/Do at different time points after dialysis and creatinine mass transfer area coefficient (MTAC) at 120min were calculated.The structures of peritoneum were observed under optical microscope and electron microscope after continuously intraperitoneal injection of Lig for 14 days.The results showed that the 90-min and 12-min creatinine D/P ratios in the group C were higher than in the group A.The 120-min creatinine MATC in the group C was higher than in the group A.The rabbits treated with Lig did not show significant structure changes of peritoneum and signs of peritoneal irritation.It was suggested that Lig could increase mass transfer ability of peritoneum without significant side effects.     

肝细胞生长因子与急性肾衰竭

肝细胞生长因子 (HGF)是一种高效的多效性因子 ,对多种器官的不同类型细胞均有多种生物学作用。HGF对于肾脏的发生、形成、修复及肾脏病理过程有重要作用 ,在急性肾衰竭 (ARF)时HGF具有促进肾小管修复及肾脏再生 ,降低死亡率 ,缩短病程的作用 ;在各种慢性肾脏疾病的发生发展中具有重要的调节作用。     

SGK1在糖尿病小鼠肾脏皮质中时间差异性表达及意义

目的：研究血清和糖皮质激素诱导的蛋白激酶1（serum and glucocorticoid-inducible kinase 1,SGK1）在糖尿病（DM）小鼠肾脏皮质中时间上差异性表达及意义。方法: 采用链脲佐菌素（STZ）单次腹腔注射诱导小鼠糖尿病模型。将2月龄C57BL/6小鼠随机分成10组：第1、2、3、4、6、8、12周糖尿病小鼠组（DM₁、DM₂、DM₃、DM₄、DM₆、DM₈、DM₁₂）和相应的第1、4、8周正常对照组（N₁、N₄、N₈）。分别在DM模型制作成功后第1、2、3、4、6、8、12周末收集小鼠24 h尿量，检测24 h尿蛋白量；观察肾脏病理改变；半定量RT-PCR检测小鼠肾脏皮质SGK1及结缔组织生长因子（CTGF）mRNA的表达，Western blotting检测N₄、DM₄、DM₈组皮质SGK1、CTGF蛋白的表达。结果: 随着糖尿病病程的进展，DM组小鼠肾小球体积逐渐增大、系膜区逐渐增宽；DM组小鼠24h尿蛋白从第2周起开始逐渐增多，肾脏皮质SGK1 mRNA表达从第2周开始明显上调，在第４周达到峰值。CTGF随着糖尿病病程的进展表达逐渐递增。结论: SGK1在糖尿病早期肾脏表达峰值的出现及CTGF 持续递增的表达，提示SGK1在糖尿病肾病肾脏纤维化的发生发展过程中起重要作用。     

Expression and Significance of Toll-like Receptor 2, 4 of Peripheral Blood Mononuclear Cells in Acute Abdomen Patients Associated with Systemic Inflammatory Response Syndrome

The changes of Toll-like receptor (TLR) 2, 4 of peripheral blood mononuclear cells (PBMCs) in the acute abdomen patients associated with systemic inflammatory response syndrome (SIRS) and their potential significance were explored. A clinical study was performed on 103 acute abdomen patients in whom 65 were associated with SIRS. Forty healthy individuals served as normal controls. The mRNA expression of TLR2, 4 was detected by RT-PCR, and the expression of TNF-αand EL-6 by ELISA. The level of plasma endotoxin, hospital stay and mortality were measured. It was found that the endotoxin level was increased to varying degrees in all the acute abdomen patients, and the endotoxin level was and hospital stay longer in SIRS group than in non-SIRS group (P<0.01). TLR2 mRNA, TLR4 mRNA, IL-6 and TNF-αcould be detected with low value in normal controls, but they were up-regulated markedly on the 1st day after admission. Then TLR4 mRNA, IL-6 and TNF-αwere decreased gradually, but TLR2 mRNA maintained at a high level till the 5th day. These indexes above in SIRS group were higher than those in non-SIRS group (P<0.01). The results of correlation analysis revealed the expression of TLR2, 4 mRNA was positively correlated with the levels of TNF-αand IL-6, and the hospital stay. The results of Logistic regression demonstrated that over-expression of TLR2, 4 mRNA might result in higher risk of multiple organ dysfunction syndrome (MODS). It was concluded that in the acute abdomen patients associated with SIRS, the expression of TLR2, 4 in PBMCs was increased markedly, suggesting that TLR might play an important role in the pathogenesis of acute abdomen associated with SIRS.     

血管内皮生长因子及其受本在先兆子痫大鼠肾损伤中的作用

目的 研究血管内皮生长因子（VEGF）及其受体（VEGFR）在先兆子痫大鼠肾损伤中的作用。方法 采用一氧化氮合酶抑制剂复制大鼠先兆子痫模型，应用原位杂交法测定肾小球VEGFmRNA转录水平，利用免疫组化法检测肾小球VEGF和VEGFR蛋白表达情况。结果 在先兆子痫大鼠中，肾小球局部VEGFmRNA和VEGF、VEGFR-2蛋白表达均增强，且表达的强度与24h尿蛋白排泄量呈正相关。结论 肾小球VEGF-VEFR系统可能参与了先兆子痫中大量蛋白尿的产生。     

诱导型一氧化氮合酶表达与获得性肾囊肿上皮恶变

诱导型一氧化氮合酶在获得性肾囊肿疾病病理诱因的作用下过度表达 ,催化产生过量一氧化氮 ,后者通过多种方式促成囊肿上皮细胞的恶变。对诱导型一氧化氮合酶表达调控及其介导的肿瘤发生、发展过程的研究有助于进一步探索获得性肾囊肿恶变机制。     

羊踯躅根对免疫复合物型肾小球肾炎核因子κB表达的影响

目的探讨核因子κB（NF-κB）在免疫复合物型肾小球肾炎发病机制中的作用；观察羊踯躅根对其表达的影响。方法采用牛血清白蛋白（BSA）方法复制免疫复合物型肾小球肾炎大鼠模型，设对照组、模型组和羊踯躅根治疗组。分别进行24h尿蛋白定量、血清肌酐检测和肾组织学检查；采用实时荧光PCR方法检测NF-κB抑制剂IκBmRNA的表达；Western blot方法检测NF-κB蛋白的表达。结果与对照组相比，治疗组和模型组的24h尿蛋白定量、血肌酐明显增加，出现异常肾组织学改变；治疗组与模型组比较，肾脏病理改变减轻，IκBmRNA降解减少，NF-κB蛋白表达下降，具有统计学意义（P〈0．01）。结论NF-κB在免疫复合物型肾小球肾炎的发病机制中扮演了重要角色，羊踯躅根制剂可能通过抑制NF-κB的激活和表达对免疫复合物型肾小球肾炎的治疗发挥作用。     

Role of Connective Tissue Growth Factor in Extracellular Matrix Degradation in Renal Tubular Epithelial Cells

In order to investigate the effects of connective tissue growth factor (CTGF) antisense oligodeoxynucleotide (ODN) on plasminogen activator inhibitor-1 (PAI-1) expression in renal tubular cells induced by transforming growth factor β1 (TGF-β1) and to explore the role of CTGF in the degradation of renal extracellular matrix (ECM), a human proximal tubular epithelial cell line (HKC) was cultured in vitro. Cationic lipid-mediated CTGF antisense ODN was transfected into HKC. After HKC were stimulated with TGF-β1 (5 μg/L), the mRNA level of PAI-1 was detected by RT-PCR. In-tracellular PAI-1 protein synthesis was assessed by flow cytometry. The secreted PAI-1 in the media was determined by Western blot. The results showed that TGF-β1 could induce tubular CTGF and PAI-1 mRNA expression. The PAI-1 mRNA expression induced by TGF-β1 was significantly inhib-ited by CTGF antisense ODN. CTGF antisense ODN also inhibited intracellular PAI-1 protein syn-thesis and lowered the levels of PAI-1 protein secreted into the media. It was concluded that CTGF might play a crucial role in the degradation of excessive ECM during tubulointerstitial fibrosis, and blocking the biological effect of CTGF may be a novel way in preventing renal fibrosis.