Background: Renal fibrosis is a frequently occurring type of chronic kidney disease that can cause end-stage renal disease. It has been verified that emodin or HGF can inhibit the development of renal fibrosis. However, the antifibrotic effect of emodin in combination with HGF remains unclear.
Methods: Cell viability was detected with CCK8. Gene and protein expression in HK2 cells was detected by qRT-PCR and Western blot, respectively. Moreover, a unilateral ureteral obstruction–induced mouse model of renal fibrosis was established for investigating the antifibrotic effect of emodin in combination with HGF in vivo.
Results: HGF notably increased the expression of collagen II in TGFβ-treated HK2 cells. In addition, HGF-induced increase in collagen II expression was further enhanced by emodin. In contrast, fibronectin, αSMA and Smad2 expression in TGFβ-stimulated HK2 cells was significantly inhibited by HGF and further decreased by combination treatment (emodin plus HGF). Moreover, we found that combination treatment exhibited better antifibrotic effects compared with emodin or HGF in vivo.
Conclusion: These data demonstrated that emodin plus HGF exhibited better antifibrotic effects compared with emodin or HGF. As such, emodin in combination with HGF may serve as a new possibilty for treatment of renal fibrosis.



中文翻译：

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大黄素通过调节 HGF 和 TGFβ-Smad 信号通路延缓肾纤维化。

背景：肾纤维化是一种常见的慢性肾病，可导致终末期肾病。已证实大黄素或HGF可抑制肾纤维化的发展。然而，大黄素与 HGF 联合的抗纤维化作用仍不清楚。
方法：用CCK8检测细胞活力。分别通过qRT-PCR和Western印迹检测HK2细胞中的基因和蛋白质表达。此外，还建立了单侧输尿管梗阻致肾纤维化小鼠模型，用于研究大黄素联合HGF的体内抗纤维化作用。
结果：HGF 显着增加了 TGFβ 处理的 HK2 细胞中胶原蛋白 II 的表达。此外，大黄素进一步增强了 HGF 诱导的胶原蛋白 II 表达的增加。相比之下，TGFβ 刺激的 HK2 细胞中纤连蛋白、αSMA 和 Smad2 的表达受到 HGF 的显着抑制，并且通过联合治疗（大黄素加 HGF）进一步降低。此外，我们发现联合治疗在体内表现出比大黄素或 HGF 更好的抗纤维化作用。
结论：这些数据表明，与大黄素或HGF相比，大黄素加HGF表现出更好的抗纤维化作用。因此，大黄素联合 HGF 可能成为治疗肾纤维化的新可能。