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Kemeng Fang 通过 PI3K/AKT 信号通路抑制膜性肾病大鼠足细胞凋亡的机制。

Mechanism of Kemeng Fang's Inhibition of Podocyte Apoptosis in Rats with Membranous Nephropathy through the PI3K/AKT Signaling Pathway.

机构信息

College of Integrated Chinese and Western Medicine, Changchun University of Chinese Medicine.

Nephropathy Department, the Affiliated Hospital to Changchun University of Chinese Medicine.

出版信息

J Vis Exp. 2024 Aug 23(210). doi: 10.3791/67170.

Abstract

Membranous nephropathy (MN) is a common pathological type of adult nephrotic syndrome. Up to 20% of patients with MN develop end-stage renal disease (ESRD). Podocytes have an important function in maintaining the glomerular filtration barrier and play a crucial role in the occurrence and development of proteinuria and MN. PI3K/AKT signaling pathway is involved in the entire process of podocyte growth, differentiation, and apoptosis. Kemeng Fang (KMF) is a traditional Chinese medicine formula that has been used to delay kidney injury. However, the therapeutic mechanism of KMF in MN is unclear. Here, the MN rat model was established by axillary, inguinal, and tail vein injections of cationized bovine serum albumin (C-BSA), and then KMF and PI3K inhibitor (LY294002) were administered. The data of liver function, kidney function, blood lipid, renal pathology, podocyte function, expression level of PI3K/AKT signaling pathway, and transcriptomics of rats demonstrated that KMF has a protective effect on the podocytes of MN rats by activating the PI3K/AKT signaling pathway, and it can effectively prevent the progression of MN.

摘要

膜性肾病(MN)是成人肾病综合征的常见病理类型。多达 20%的 MN 患者发展为终末期肾病(ESRD)。足细胞在维持肾小球滤过屏障方面具有重要功能,在蛋白尿和 MN 的发生发展中起着关键作用。PI3K/AKT 信号通路参与足细胞生长、分化和凋亡的全过程。抗纤溶酶方(KMF)是一种已被用于延缓肾损伤的中药方剂。然而,KMF 在 MN 中的治疗机制尚不清楚。本研究通过腋、腹股沟和尾静脉注射阳离子化牛血清白蛋白(C-BSA)建立 MN 大鼠模型,然后给予 KMF 和 PI3K 抑制剂(LY294002)。大鼠的肝功能、肾功能、血脂、肾脏病理、足细胞功能、PI3K/AKT 信号通路表达水平和转录组学数据表明,KMF 通过激活 PI3K/AKT 信号通路对 MN 大鼠的足细胞具有保护作用,并能有效阻止 MN 的进展。

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