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首页> 外文期刊>Clinical and experimental pharmacology & physiology >Opposite actions of urotensin II and relaxin‐2 on cellular expression of fibronectin in renal fibrosis: A preliminary experimental study
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Opposite actions of urotensin II and relaxin‐2 on cellular expression of fibronectin in renal fibrosis: A preliminary experimental study

机译:尿肾上腺素II和弛豫素-2对肾纤维化纤维素细胞表达的相反作用:初步实验研究

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Summary Our aim was to evaluate the role of urotensin II , urantide (urotensin II receptor antagonist) and relaxin‐2 on the cellular expression of fibronectin as a surrogate marker for renal fibrosis. We employed LLC ‐ PK 1 renal tubular epithelial cells and assessed the influence on the fibrotic process of the above‐mentioned substances by using anti‐fibronectin antibodies in western blot analysis. The addition of urotensin II increased fibronectin expression. Urantide reduced the positivity for fibronectin caused by urotensin II ( P .05). The anti‐fibrotic action was more evident for relaxin‐2 ( P .01). Also in the model of TGF ‐β1‐induced fibrosis, urantide and, to a greater extent, relaxin‐2 were able to significantly lessen fibronectin expression (respectively, P .05 and P .01). In conclusion, relaxin‐2 may reduce urotensin II ‐induced renal fibrosis.
机译:总结我们的目的是评估尿黄素II,尿素II,尿素(尿肾上腺素II受体拮抗剂)和弛豫素-2对纤维素的细胞表达作为肾纤维化的替代标志物的作用。 我们使用LLC - PK 1肾小管上皮细胞,并通过使用蛋白质印迹分析中的抗纤连蛋白抗体评估对上述物质的纤维化过程的影响。 添加尿黄素II增加了纤连蛋白表达。 铀素II(P <0.05)引起的纤连蛋白的阳性降低了纤连蛋白的阳性。 对弛豫素-2(P <.01)更明显的抗纤维化作用。 同样在TGF-β1诱导的纤维化,芳antidide的模型中,在更大程度上,弛豫素-2能够显着减少纤连蛋白表达(分别,P <.05和P <.01)。 总之,放松素-2可降低尿溶素II〜肾纤维化。

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