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首页> 外文期刊>Journal of Cellular Physiology >Metformin attenuates folic‐acid induced renal fibrosis in mice
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Metformin attenuates folic‐acid induced renal fibrosis in mice

机译：二甲双胍叶酸量酸诱导肾变弱的问题纤维化小鼠

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Progressive tubulointerstitial fibrosis has been recognized as a common pathological process that leads to the progression of all chronic kidney disease (CKD). Innovative strategies are needed to both prevent and treat CKD. Inflammatory and fibrotic signaling pathways play central roles in the progression of CKD regardless of aetiology. Hence, targeting inflammatory and fibrotic responses holds promise to limit renal fibrosis. Metformin has been the most prescribed glucose‐lowering medicine worldwide, and its potential for many other therapeutic applications is also being explored intensively. Increasing evidence indicates metformin may limit renal fibrosis. However, the exact mechanisms whereby metformin limits renal injury are not fully understood. The anti‐fibrotic effects of metformin, independent of improved glycaemic control was examined in a folic acid‐induced mouse model of nephropathy for 14 days. Human proximal tubular cells (HK2 cells) exposed to TGF‐β1 were used in in vitro models to examine mechanistic pathways. Folic acid induced nephropathy was associated with the overexpression of inflammatory markers MCP‐1, F4/80, type IV collagen, fibronectin and TGF‐β1 compared to control groups, which were partially attenuated by metformin treatment. In vitro studies confirmed that metformin inhibited TGF‐β1 induced inflammatory and fibrotic responses through Smad3, ERK1/2, and P38 pathways in human renal proximal tubular cells. These results suggest that metoformin attenuates folic acid‐induced renal interstitial fibrogenesis through TGF‐β1 signaling pathways.
机译：阻力指标纤维化也许可以进步被认为是一种常见的病理过程,导致所有慢性肾脏的进展疾病(CKD)。预防和治疗慢性肾病。纤维化信号通路中扮演中心角色CKD不管病因学的发展。因此,针对炎症和纤维化肾纤维化反应持有承诺限制。二甲双胍是最开葡萄糖量降低药物在世界范围内,和它的对于许多其它治疗的应用潜力也正在探索集中。证据显示二甲双胍可能限制肾纤维化二甲双胍限制肾损伤并不充分理解。二甲双胍,独立于改善血糖控制检查在叶酸的诱导小鼠模型的肾病14天。近端小管细胞(HK2细胞)接触地理TGFβ1被用于体外模型研究机械化的途径。肾病是相关的过度的炎症标志物MCP高1F4/80, IV型胶原蛋白、纤连蛋白和TGFβ1与对照组相比,部分减毒的二甲双胍治疗。研究证实,二甲双胍抑制TGFβ1诱导炎症和纤维化反应通过Smad3 ERK1/2和P38通路在人类肾近端小管细胞。表明metoformin减弱叶酸酸诱导肾间质纤维发生通过转化生长因子β1信号通路。

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