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Objective To investigate the role and mechanism of phosphate myosin light chain (pMLC) in the rat kidney of chronic allograft nephropathy (CAN) model. Methods The left donor kidneys from Fisher (F344) rats were orthotopically transplanted into Lewis recipients. Meanwhile, the F344 rats and LEW rats with resection of the right kidney served as control groups. Animals were harvested respectively at the 4th, 8th and 12th week after transplantation. The creatinine clearance rate (CCr) was calculated by urine creatinine of 24-h urine. Blood samples were collected from rats for determination of serum creatinine. The expression of pMLC was detected by using Western blotting and immunohistochernistry, and that of integrin-linked kinase (ILK) by using immunohistochemistry. Results Mononuclear cells infiltration of allografts was markedly aggravated as compared to the controls. Allografts got severe interstitial fibrosis and tubular atrophy at 12th week after transplantation. The expression of pMILC and ILK was up-regulated in the kidney of CAN rats after transplantation, and increased more significantly as the time went on. The expression of pMILC was significantly correlated with 24-h urine protein excretion (r= 0. 273, P＜0. 05), serum creatinine levels (r = 0. 434, P＜0. 01 ), the number of tubulointerstitial infiltrated mononuclear cells (r = 0. 525, P＜0. 01 ), the number of smooth muscle cells (SMC) in vascular wall (r= 0. 676, P＜0. 01 ) and the extent of interstitial fibrosis (r= 0. 570, P＜0. 01 ).There was a significantly positive correlation between ILK and pMLC in CAN rats at the 4th week after transplantation (r= 0. 778, P＜0. 01 ). Conclusion pMLC might play an key role in CAN, and the over-expression of ILK might be involve in the pathogenesis of CAN.
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Objective To investigate the expression and significance of glucogen synthase kinase-3β (GSK-3β) in the pathogenesis of chronic allograft nephropathy (CAN) in rats.Methods Kidneys of Fisher (F344) rats as donors were orthotopically transplanted into Lewis (LEW) rats as recipients.The renal function and histopathological changes were observed at 4,8,12,16,and 24week post-transplantation.Phosphorylated GSK-3β (p-GSK-3β) protein and mRNA expression was determined by using immunohistological assays and RT-PCR respectively.Results Our data showed that 24-h urinary protein excretion in CAN rats was increased significantly at week 16 as compared with F344/LEW controls.Allografts showed markedly increased mononuclear cells infiltration and presented with severe interstitial fibrosis and tubular atrophy at 16 and 24 week post-transplantation.p-GSK-3β expression (protein/mRNA) was down-regulated in rat kidneys with CAN,and the decrease became more significant over time after transplantation.p-GSK-3β expression was correlated significantly with 24-h urinary protein excretion,serum creatinine levels,tubulointerstitial mononuclear cells infiltration,smooth muscle cells migration in vascular wall,and interstitial fibrosis.Conclusion It was concluded that GSK-3β down-regulation was the key event that may be involved in mononuclear cells infiltration and vascular SMCs migration at early stage,and interstitial fibrosis and allograft nephroangiosclerosis at later stage of CAN pathogenesis in rats.
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Objective To investigate the effect of apolipoprotein E (ApoE) gene polymorphism on lipid metabolism of renal transplant recipients before and after transplantation. Methods ApoE gene polymorphism was detected by Polymerase chain reaction restriction fragment length polymorphism and serum lipid levels were measured by biochemical method. Results Serum lipid levels in the recipients were increased significantly at 3rd month after renal transplantation, and were ulteriorly elevated at 6 th month and the first year. The patients with higher total serum cholesterol (TC) and triglyceride (TG) levels were only accounted for 2.9 % and 7.6 % respectively before renal transplantation, but for 28.6 % and 46.7 % respectively at 3rd month after renal transplantation ( P
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Objective To discuss the clinical values of 18 F-FDG imaging in screening of the recipients with liver transplantation.Methods By using positron emission tomography, 16 case of hepatocellular carcinoma and 21 case of hepatic cirrhosis with discompensation were subjected to 18 F-FDG imaging. The obtained images were fused with CT images. According to the result of the abnormal 18 F-FDG uptake in 18 F-FDG imaging and image fusion with CT imaging, extrahepatic malignant tumor was judged. The initial routine examinations showed no extrahepatic malignant tumor in these 37 cases , including primary extrahepatic carcinoma and extrahepatic metastasis of liver carcinoma.Results Among the 21 case of hepatic cirrhosis with discompensation, there were 5 cases of extrahepatic primary carcinoma and metastasis. In 16 cases of primary hepatocellular carcinoma, there were 7 cases of extrahepatic metastasis.Conclusion 18 F-FDG positron emission tomography imaging can find the extrahepatic carcinomas which can not be discovered by other examinations, which can provide more information for screening of the recipients undergoing liver transplantation.
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Objective To explore the influence of MMF on the presentation functions of in vitro cultured dendritic cells.Methods Bone marrow-derived dendritic cell progenitors from BalB/c mice were treated with MMF or without. The antigen-presenting capacities, antigen specific proliferation reaction, mixed lymphocyte reaction and antigen-specific hyporesponsiveness of T-cells were analyzed to investigate the influences of MMF on the presentation functions of dendritic cells.Results Treatment with MMF reduced the soluble antigen presenting capacities of DCs to T cells. The proliferation of syngeneic T cells co-cultured with MMF-DC was significantly depressed, and displayed a comparatively low level of MLR-sti- mulatory activity. The levels of T helper cells derived cytokines were depressed, too.Conclusion MMF has a suppressive influences on the antigen-presenting functions of in vitro cultured dendritic cells and promotes the tolerance-induction effect of DCp.