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Laminins Expression in Children with Mesangial Proliferative Glomerulonephritis
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作者 赵非 黄松明 +3 位作者 陈荣华 费莉 郭梅 黄文彦 《Journal of Nanjing Medical University》 2003年第5期237-242,共6页
Objective: To investigate the role of laminins in the pathogensis of mesangial pro-liferative glomeruonephritis (MsPGN) in children. Methods: Eighteen renal biopsy specimens of MsPGN and 6 normal kidneys were studied ... Objective: To investigate the role of laminins in the pathogensis of mesangial pro-liferative glomeruonephritis (MsPGN) in children. Methods: Eighteen renal biopsy specimens of MsPGN and 6 normal kidneys were studied by means of immunohistochemistry and in situ hybridization. Results: ① Protein of α1 chain and γ1 chain of laminin increased around the segments of prolifera-tive mesangium. Increased expression of α2 and β1 proteins was found in the segments with mesangial proliferation whereas the β2 chain expression decreased in these areas. ② The mRNA expression of α1, α2, β1 and γ1 increased to different degrees in glomeruli with mesangial proliferation. But no difference was detected among Mild, Moderate, and Severe MsPGN. Conclusion:① The quantitative and qualitative alterations of laminin chains' distribution were found in the measngial proliferative glomeruli. The proliferative mesangial cells were the origins of abnormal accumulation and expression of laminins. ② These changes may be the basis of the progresses of MsPGN. 展开更多
关键词 LAMININ mesangial proliferative glomeruonephritis immunohistoche-mistry in situ hybridization
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Effects of GTW treatment on proteinuria and acute glomerular immune lesion in experimental mesangial proliferative glomerulonephritis
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作者 YI GANG WAN WEI SUN 《Journal of Microbiology and Immunology》 2005年第3期165-173,共9页
To examine the effect of multi-glycoside of Tripterygium wilfordii Hook. f. (GTW) on proteinuria and acute glomerular immune lesion in experimental mesangial proliferative glomerulonephritis (MsPGN) induced by ant... To examine the effect of multi-glycoside of Tripterygium wilfordii Hook. f. (GTW) on proteinuria and acute glomerular immune lesion in experimental mesangial proliferative glomerulonephritis (MsPGN) induced by anti-Thyl. 1 monoelonal antibody (mAb) 1-22-3. The reversible model of MsPGN with anti-Thyl. 1 mAb 1-22-3 was established. After 7 days of oral treatment with GTW ( 100 mg/kg per day) and vehicle (distilled water, 5 ml/kg per day), its effects on proteinuria, renal functions, mesangial morphological change, glomerular macrophage accumulation, and mRNA expressions of cytokines (PDGF-BB and MCP-1 ) were evaluated by light microscope (LM), immunofluorescence (IF), and reverse transcription polymerase chain reaction (RT-PCR). It was found that GTW ameliorated proteinuria (on day 3 and day 7), mesangial proliferation (total cell number, matrix expansion, a-smooth muscle actin expression, and collagen type Ⅰ expression) and macrophage accumulation (ED3^+ ) in experimental MsPGN. In addition, GTW significantly suppressed the increased mRNA expressions for MCP-1 (67.6% to eontrol group, P 〈 0.01) together with the tendency to reduce the expression of PDGF (24.44% to control group) on day 7. It is concluded that GTW can not only decrease proteinuria, but also ameliorate acute mesangial alterations and glomerular activated macrophage accumulation probably by reduction of cytokines. These data indicate that GTW is an effective agent for early MsPGN. 展开更多
关键词 Multi-glycoside of Tripterygium wilfordii Hook .f. (GTW) mesangial proliferative glomerulonephritis (MsPGN) Cytokine mesangial proliferation Macrophage accumulation
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Changes in renal function and morphological variations of kidney diseases in rheumatoid arthritis patients
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作者 Yan Tang Yuliya Varavko +1 位作者 Raisa Aringazina Irina Menshikova 《Asian Journal of Urology》 CSCD 2024年第2期304-310,共7页
Objective:Rheumatoid nephropathy is one of the most severe extra-articular manifestations of rheumatoid arthritis(RA)associated with a very unfavorable prognosis.This study aimed to identify changes in renal function ... Objective:Rheumatoid nephropathy is one of the most severe extra-articular manifestations of rheumatoid arthritis(RA)associated with a very unfavorable prognosis.This study aimed to identify changes in renal function and morphological variations of kidney diseases in RA patients.Methods:The study enrolled patients(126 patients)between 18 and 55 years of age with a confirmed active RA of more than 12 months.Each patient underwent the following range of laboratory and instrumental research methods:general clinical analysis of blood and urine,performing urinalysis according to Nechiporenko method;determining daily proteinuria;determining the blood content of glucose,urea,creatinine,uric acid,total bilirubin,liver transaminase level,ionogram,lipidogram,and coagulogram;determining the blood content of rheumatoid factor,anti-streptolysin O,and C-reactive protein;and X-ray of the joints of hands and feet.Renal function was examined by estimating glomerular filtration rate,tubular reabsorption index,and renal functional reserve.For studying the morphological changes in the kidneys under ultrasound examination,renal biopsy was performed in 31 patients with RA with urinary syndrome(proteinuria more than 0.3 g per day and hematuria).Results:Nephropathy in RA is characterized by impaired renal function and manifested by an increased blood creatinine and a decrease in glomerular filtration rate and renal functional reserve.Among morphological variations of nephropathy at RA,mesangial proliferative glomerulonephritis prevails,accounting for 48.4%of patients.Other disorders include the secondary amyloidosis(29.0%of patients),tubulointerstitial nephritis(16.1%),membranous glomerulonephritis(3.2%),and focal-segmental glomerulosclerosis(3.2%).Conclusion:Kidney damage is a common systemic manifestation of RA with a long and active course,a major nephropathy trigger. 展开更多
关键词 Rheumatoid nephropathy Secondaryrenal amyloidosis mesangial proliferative glomerulonephritis Renal functional reserve
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The role of transcriptional factor D-site-binding protein in circadian CCL2 gene expression in anti-Thy1 nephritis 被引量:7
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作者 Yang Lu Yan Mei +10 位作者 Lei Chen Lingling Wu Xu Wang Yingjie Zhang Bo Fu Xizhao Chen Yuansheng Xie Guangyan Cai Xueyuan Bai Qinggang Li Xiangmei Chen 《Cellular & Molecular Immunology》 SCIE CAS CSCD 2019年第9期735-745,共11页
Mesangial proliferative glomerulonephritis(MsPGN)is an inflammatory disease,but both the nature of disease progression and its regulation remain unclear.In the present study,we monitored the course of anti-Thy1 nephri... Mesangial proliferative glomerulonephritis(MsPGN)is an inflammatory disease,but both the nature of disease progression and its regulation remain unclear.In the present study,we monitored the course of anti-Thy1 nephritis from days 1 to 5 and established gene expression profiles at each time point using microarrays to explore the development of inflammation.According to the gene expression profiles,macrophage infiltration(triggered by CCL2 activation)was evident on day 1 and enhanced inflammation over the next few days.We screened for genes with expression levels similar to CCL2 and found that the upregulation of the circadian gene albumin D-site-binding protein(DBP)was involved in CCL2 activation in mesangial cells.More importantly,CCL2 expression showed oscillatory changes similar to DBP,and DBP induced peak CCL2 expression at 16:00 a clock on day 1 in the anti-Thy1 nephritis model.We knocked down DBP through transfection with a small interfering RNA(siRNA)and used RNA sequencing to identify the DBP-regulated TNF-α-CCL2 pathway.We performed chromatin immunoprecipitation sequencing(ChIP-Seq)and the dual luciferase assay to show that DBP bound to the TRIM55 promoter,regulating gene expression and in turn controlling the TNF-α-CCL2 pathway.In conclusion,DBP-regulated circadian CCL2 expression by the TRIM55-TNF pathway in injured mesangial cells at an early stage,which promoted macrophage recruitment and in turn triggered infiltration and inflammation in a model of anti-Thy1 nephritis. 展开更多
关键词 mesangial proliferative glomerulonephritis DBP CCL2 Trim 55 Macrophage
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