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1.
Chinese Journal of Tissue Engineering Research ; (53): 858-861, 2010.
Artigo em Chinês | WPRIM | ID: wpr-403494

RESUMO

BACKGROUND: It has confirmed that angiotensin converting enzyme inhibitor benazepril can delay fibrosis of varied organs. However, whether benazepril has inhabited effect on peritoneal fibrosis in the process of peritoneal dialysis is poorly understood. OBJECTIVE: It is assumed that benazepril could inhabit peritoneal fibrosis of peritoneum with peritoneal dialysis, in addition, to compare the effect to other mehods. METHODS: All rats were randomly and evenly divided into 4 groups. There was no intervention in the control group; saline solution, and 20 mL 42.5 g/L Dianeal solution, was injected into rats in the saline solution and peritoneal dialysis groups; in the combination group, 20 mL 42.5 g/L Dianeal solution was injected combined with oral taken benazepril 20 mg/(kg·d). The intraperitoneal injection performed once a day, for 4 successive weeks. The ultrafiltration function was performed 4 weeks later. Meantime, Paraffin sections were cut and stained by Van Gieson to measure peritoneal thickness. RESULTS AND CONCLUSION: Two rats in the peritoneal dialysis group and 1 rat in the combination group were dead. The remained 37 rats were included in the final analysis. Compared to the control and saline solution groups, the ultrafiltration volume of the peritoneal dialysis and combination groups were obviously decreased (P_(all)< 0.05), especially notably decreased in the combination group (P< 0.05). Compared to the control group end saline solution groups, the peritoneal thickness was significantly elevated in the combination group, but not as much as in the peritoneal dialysis group (P < 0.05). In the long-term peritoneal dialysis rats, administration of benazepril can effectively protect the ultrofiltration function of peritoneum and delay the progression of peritoneal fibrosis.

2.
Journal of Experimental Hematology ; (6): 129-132, 2000.
Artigo em Chinês | WPRIM | ID: wpr-354924

RESUMO

The effectiveness of rhIL-11 on thrombocytopenia induced by carboplatin in rhesus monkeys was investigated. Thrombocytopenia was induced in monkeys by i.v. administration of carboplatin at a dose of 15 mg/kg(-1)/d(-1) for three consecutive days. rhIL-11 (50 or 100 micro g/kg(-1)/d(-1)) or Neumega (100 micro g/kg(-1)/d(-1)) were administered s.c. for 14 days beginning one day following the final dose of carboplatin. The results showed that rhIL-11 significantly improved mean platelet nadirs and shortened the mean duration of platelet counts less than 50% of pre-treatment values. Administration of rhIL-11 also resulted in moderate increase of the reticulated platelet, leukocyte and reticulocyte counts in peripheral blood and megakaryocytic and erythroid progenitors in bone marrow. rhIL-11 did not enhance ADP-induced platelet aggregation. These results indicate that rhIL-11 has a potent thrombopoietic effect in vivo and could be an important agent to reduce the severity and duration of thrombocytopenia following chemotherapy.

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