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1.
Oncol Lett ; 14(1): 137-144, 2017 Jul.
Artigo em Inglês | MEDLINE | ID: mdl-28693145

RESUMO

The aim of the current study was to investigate the chromosomal aberrations of exfoliated bladder cells in the urine and blood oxidative stress in patients with bladder transitional cell carcinoma (BTCC). A total of 40 healthy controls and 246 patients with BTCC were recruited. Abnormal levels of CSP3, CSP7, CSP17 and GLPp16 were detected by fluorescence in situ hybridization (FISH) in exfoliated bladder cells in the urine of patients with BTCC. Serum total oxidant status (TOS), total antioxidant status (TAS) and oxidative stress index (OSI) were measured. Significant differences were observed in the abnormal CSP3, CSP7, CSP17, GLPp16 signals and FISH positive rate between patients with BTCC and healthy controls (P<0.001). Serum TOS, TAS and OSI were also significantly different between the two groups (P<0.001). The clinical stage of BTCC was not associated with abnormal CSP3, CSP7, CSP17, GLPp16 or FISH positive rate and oxidative stress (P>0.05). A Gamma rank correlation analysis revealed an association between the pathological grade of BTCC with abnormal CSP3, CSP7 and CSP17 as well as FISH positive rate (P<0.001). In addition, the clinical stage of BTCC was associated with serum TOS, TAS and OSI (P<0.001). Evaluation of the association between chromosomal aberrations and oxidative stress revealed that abnormal CSP3, CSP7 and CSP17 were positively associated with serum TOS and OSI (P<0.001), abnormal CSP7 and CSP17 were negatively associated with serum TAS (P<0.001), but abnormal GLPp16 was not associated with serum TOS, TAS or OSI (P>0.05). Therefore, the chromosomal aberrations of exfoliated bladder cells in the urine are associated with blood oxidative stress in patients with BTCC, and these factors may contribute to the occurrence and development of BTCC.

2.
Sichuan Da Xue Xue Bao Yi Xue Ban ; 38(6): 918-23, 2007 Nov.
Artigo em Chinês | MEDLINE | ID: mdl-18095586

RESUMO

OBJECTIVE: This study is aiming to investigate the mechanism and drug intervention of chronic allograft nephropathy (CAN) induced by renal ischemia-reperfusion injury. METHODS: The closed colony strain Sprague-Dawley (SD) and Wistar Rats were used as donor and recipient, respectively. Orthotopic kidney transplantation was performed following the procedure of our previous study. The rats were divided into five groups: Group A only received CsA with 10 mg/(kg x d); except CsA, Group B,C,D received Yi Sheng injection with 4 mg/(kg x d), 8 mg/(kg x d), and MMF (20 mg/(kg x d)], respectively. Group E was control group. According to Banff standard, the serum creatinine (SCr) level and pathological change of rat grafted kidney were observed at the 4th, 8th and 12th weeks post-transplantation. The immunohistochemistry and real-time fluorescence quantitative polymerase chain reaction were used to comprehend the localization and expression of TGFbeta1 and Smad2, 7 in the transplant kidney. RESULTS: Compared with the lower dosage group, the differences of SCr level and pathological changes of CAN at all the time points after 8th week were statistically significant in the high dosage Yi Sheng group. It was showed that the Yi Sheng injection had the protective effect on CAN with a dose-dependent fashion. After transplantation, the rat kidney-sclerosis model showed that the up-regulated expressions of TGF-P, and Smad2 and the down-regulated expression of Smad7 in Group A and Group B were statistically significant, which meant that the difference was obvious when Group A compared with the other 4 groups. The expressions of TGF-beta1, and Smad2 were strongly positive in tubular epithelial cell, interstitial cell and glomerulus, while the expression of Smad7 was weak. Thickening of endovascular could significantly be inhibited in high dosage of Yi Sheng and MMF group. CONCLUSION: The up-regulated expressions of TGF-beta1 and Smad2 and the down-regulated expression of Smad7 may accelerate the progression of CAN alone or with immune factors. The traditional Chinese medicine Yi Sheng injection and MMF can down-regulate the expression of TGF-beta1 and Smad2 and block the down-regulated expression of Smad7, which may postpone and lessen the progression of CAN.


Assuntos
Medicamentos de Ervas Chinesas/uso terapêutico , Nefropatias/tratamento farmacológico , Transplante de Rim/efeitos adversos , Ácido Micofenólico/análogos & derivados , Traumatismo por Reperfusão/patologia , Animais , Relação Dose-Resposta a Droga , Regulação da Expressão Gênica , Imunossupressores/uso terapêutico , Rim/patologia , Ácido Micofenólico/uso terapêutico , Ratos , Ratos Sprague-Dawley , Ratos Wistar , Proteína Smad2/metabolismo , Proteína Smad7/metabolismo , Fator de Crescimento Transformador beta1/metabolismo , Transplante Homólogo
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