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Involvement of cytokines in the modulation and progression of renal fibrosis induced by unilateral ureteral obstruction in C57BL/6 mice: effects of thalidomide and dexamethasone

肌酐 血尿素氮 内科学 地塞米松 医学 内分泌学 纤维化 肾功能 促炎细胞因子 炎症
作者
Luiz Eduardo Bersani‐Amado,Jailson Araújo Dantas,Márcio José Damião,Bruno Ambrósio da Rocha,Jean Carlos Fernando Besson,Rafael Lucena Bastos,Letícia Nicoletti Silva,Ciomar Aparecida Bersani‐Amado,Roberto Kenji Nakamura Cuman
出处
期刊:Fundamental & Clinical Pharmacology [Wiley]
卷期号:30 (1): 35-46 被引量:11
标识
DOI:10.1111/fcp.12162
摘要

Abstract This study investigated the kinetics of cytokines that are involved in the development of interstitial fibrosis in mice that were subjected to UUO , the interstitial type I and III collagen deposition, and the effects of Thalido and Dexa treatment on these parameters. Inbred C57 BL /6 mice were divided into the groups: Normal (not submitted surgery), Sham (sham surgery), Control ( UUO treated with 0.5% carboxymethyl cellulose), Thalido ( UUO treated with 5 mg/kg thalidomide), and Dexa ( UUO treated with 1 mg/kg dexamethasone). The treatments began the day before surgery and were administered once daily by gavage for 1, 7, or 14 days. At the end of each treatment period, blood samples were collected for the determination of creatinine, urea, cytokines. The Control group exhibited a increase in creatinine concentration compared with the Normal and Sham groups within the first 24 h after UUO , which remained high until days 7 and 14. The urea concentration was higher on days 7 and 14 in the Control group compared with the Sham group. In the Thalido and Dexa groups, a reduction of serum creatinine concentration was seen on day 14. Treatment with Dexa reduced the serum concentration of urea on day 7. The serum concentrations of cytokines ( TNF ‐α, IL ‐1β, IL ‐6, IL ‐10 and IL ‐17) and chemokines ( KC , MIG , bFGF ) increased in UUO mice at all of the sampling times. The Dexa and Thalido groups exhibited alterations in the concentrations of these cytokines, suggesting the involvement of anti‐inflammatory and immunomodulatory mechanisms that may have modified the fibrosis framework.
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