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Fu-Fang-Jin-Qian-Cao herbal granules protect against the calcium oxalate-induced renal EMT by inhibiting the TGF-β/smad pathway

机译:通过抑制TGF-β/ SMAD途径,富芳金 - 曹 - 曹曹草药颗粒防止草酸钙诱导的肾功能

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Context Nephrolithiasis is a major public health problem worldwide and Fu-Fang-Jin-Qian-Cao granules (FFJQC) is a traditional Chinese herbal formula that is used to treat nephrolithiasis. The main component of nephrolithiasis is calcium oxalate (CaOx) and the epithelial-mesenchymal transition (EMT) shown to play a crucial role in CaOx-induced kidney injury. However, the mechanism underlying the therapeutic effect of FFJQC on the CaOx-induced renal EMT is unknown. Objective This study explores the therapeutic benefits and mechanism of FFJQC in oxalate-induced kidney injury. Materials and methods 60 male C57BL/6 mice were used in this experiment and divided into 6 groups. A mouse kidney stone model was created by intraperitoneal injection of glyoxylate at a dose of 100?mg/kg for 6?days. The standardized FFJQC was used to treat mouse crystal kidney injury by gavage at 1.35 and 2.7?g/kg, respectively. Western blotting and immunostaining for E-cadherin, cytokeratin 18 (CK18), vimentin, smooth muscle α-actin (α-SMA) and transforming growth factor β (TGF-β)/Smad pathway were conducted on renal tissues. Results Following CaOx-induced kidney injury, the levels of E-cadherin and CK18 in kidney decreased, while vimentin and α-SMA levels increased. The FFJQC treatment increased the levels of E-cadherin and CK18 and decreased vimentin and α-SMA levels in varying degrees. What’s more, the FFJQC reduced the expression of CaOx-induced fibrosis marker collagen II. Conclusion FFJQC alleviated the CaOx-induced renal EMT and fibrosis by regulating TGF-β/smad pathway. Therefore, the FFJQC is an important traditional Chinese medicine for the treatment of CaOx-induced renal injury and fibrosis.
机译:背景上肾血红病是一个主要的公共卫生问题,富芳金 - 钱 - 曹颗粒(FFJQC)是一种用于治疗肾病性的中药配方。肾状二病原的主要成分是草酸钙(CAOX)和上皮 - 间充质转换(EMT),显示在曹陶诱导的肾损伤中发挥至关重要的作用。然而,FFJQC在曹焦诱导的肾EMT上的治疗作用的机制是未知的。目的本研究探讨了FFJQC在草酸盐诱导的肾损伤中的治疗益处和机制。材料和方法在该实验中使用60只雄性C57BL / 6小鼠,分为6组。通过以100μmg/ kg的剂量为6〜天的剂量注射糖细胞内注射糖细胞的糖细酸肾上腺素。标准化的FFJQC分别用于在1.35和2.7?G / kg下通过饲料治疗小鼠晶体肾损伤。对肾组织进行了对E-Cadherin,细胞角蛋白,细胞角蛋白,细胞角蛋白18(CK18),Vimentin,平滑肌α-肌动蛋白(α-SMA)和转化生长因子β(TGF-β)/ smad途径的免疫印迹和免疫抑制。结果曹兴诱导的肾损伤后,肾脏肝蛋白和CK18的水平降低,而Vimentin和α-SMA水平增加。 FFJQC治疗增加了e-cadherin和CK18的水平,并且降低了不同程度的Vimentin和α-SMA水平。更重要的是,FFJQC降低了曹兴诱导的纤维化标志物胶原II的表达。结论FFJQC通过调节TGF-β/ Smad途径来缓解CAOX诱导的肾EMT和纤维化。因此,FFJQC是一种重要的中药,用于治疗Caox诱导的肾损伤和纤维化。

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