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首页> 外文期刊>American Journal of Physiology >SMP-534 ameliorates progression of glomerular fibrosis and urinary albumin in diabetic db/db mice.
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SMP-534 ameliorates progression of glomerular fibrosis and urinary albumin in diabetic db/db mice.

机译：SMP-534改善了糖尿病db / db小鼠的肾小球纤维化和尿白蛋白的进展。

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Diabetic nephropathy is currently the most common cause of end-stage renal disease. Diabetic nephropathy patients, whether insulin dependent or not, develop fibrotic changes in glomeruli that manifest as overt nephropathy. Previously, we demonstrated that 5-chloro-2-{(1E)-3-[2-(4-methoxybenzoyl)-4-methyl-1H-pyrrol-1-yl]prop-1-en -1-yl}-N-(methylsulfonyl)benzamide (SMP-534) reduces extracellular matrix (ECM) production induced by transforming growth factor-beta (TGF-beta) in vitro and prevents the accumulation of ECM in glomeruli in rat Thy-1 nephritis models. In this study, we examined the long-term effects of SMP-534 on renal insufficiency and glomerulosclerosis in db/db mice, which are models of type 2 diabetes. A diet containing SMP-534 was given to the mice from the age of 9 to 25 wk, and blood and urine analysis were performed at 8, 17, and 25 wk. At the end of study, kidney tissues were analyzed histologically. Treatment with SMP-534 dose dependently suppressed the increase of urinary albumin andtype IV collagen excretion in db/db mice. The renal histological analysis showed that SMP-534 dose dependently suppressed the increase of mesangial expansion in the kidney. In the immunohistological analysis, fibronectin and type IV collagen expression were lower in SMP-534-treated db/db mice compared with vehicle-treated db/db mice. This study suggested that SMP-534 ameliorated the increase of ECM production in kidney of db/db mice, possibly through the inhibition of TGF-beta action. Hence, antifibrotic agents such as SMP-534 might be a new therapeutic option for the treatment of diabetic nephropathy.
机译：糖尿病肾病目前是终末期肾脏疾病的最常见原因。糖尿病性肾病患者，无论是否依赖胰岛素​​，都会出现肾小球纤维化改变，表现为明显的肾病。以前，我们证明了5-chloro-2-{（1E）-3- [2-（4-甲氧基苯甲酰基）-4-甲基-1H-吡咯-1-基] prop-1-en -1-yl}- N-（甲基磺酰基）苯甲酰胺（SMP-534）在体外可降低大鼠Thy-1肾炎模型中转化生长因子-β（TGF-β）诱导的细胞外基质（ECM）的产生，并防止ECM在肾小球中积聚。在这项研究中，我们检查了SMP-534对db / db小鼠（这是2型糖尿病的模型）的肾功能不全和肾小球硬化的长期影响。在9至25周之间给小鼠添加了含SMP-534的饮食，并在8、17和25周进行了血液和尿液分析。在研究结束时，对肾脏组织进行组织学分析。用SMP-534处理可剂量依赖性地抑制db / db小鼠尿白蛋白的增加和IV型胶原蛋白的排泄。肾脏组织学分析表明，SMP-534剂量依赖性地抑制了肾小球系膜扩张的增加。在免疫组织学分析中，与媒介物处理的db / db小鼠相比，经SMP-534处理的db / db小鼠的纤连蛋白和IV型胶原表达较低。这项研究表明，SMP-534可能通过抑制TGF-β的作用改善了db / db小鼠肾脏中ECM的产生。因此，抗纤维化剂如SMP-534可能是治疗糖尿病性肾病的新治疗选择。

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