Brahma‐related gene 1 (Brg‐1) is perceived as a cytoprotective protein due to its role in alleviating oxidative stress and apoptosis. Our study aimed to explore the role and mechanism of Brg‐1 in high glucose (HG)‐stimulated podocytes. The HG exposure downregulated Brg‐1 and inactivated the protein kinase B (Akt) pathway in podocytes. Restoration of Brg‐1 inhibited HG‐induced viability reduction of podocytes. The HG‐induced increase of reactive oxygen species and malondialdehyde levels and decrease of superoxide dismutase activity in podocytes were reversed by the Brg‐1 overexpression. The Brg‐1 overexpression terminated the HG‐induced production of fibronectin, collagen IV, transforming growth factor‐β1, and connective tissue growth factor. In addition, the Brg‐1 overexpression activated Akt‐dependent nuclear factor E2‐related factor 2 (Nrf2)/antioxidant response element (ARE) signaling in HG‐stimulated podocytes. However, inhibition of the Akt pathway or Nrf2 silencing counteracted the protective effects of Brg‐1 in HG‐stimulated podocytes. In conclusion, the Brg‐1 overexpression suppressed HG‐induced oxidative stress and extracellular matrix accumulation by activation of Akt‐dependent Nrf2/ARE signaling in podocytes.

中文翻译：

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通过恢复Brg-1来激活Akt依赖的Nrf2 / ARE途径可以缓解高葡萄糖诱导的氧化应激和足细胞中的ECM积累

婆罗门相关基因1（Brg-1）被认为是一种细胞保护蛋白，因为它在减轻氧化应激和凋亡方面具有重要作用。我们的研究旨在探讨Brg-1在高葡萄糖（HG）刺激的足细胞中的作用和机制。HG暴露下调了足细胞中的Brg-1，并使蛋白激酶B（Akt）通路失活。Brg-1的恢复抑制了HG诱导的足细胞活力降低。HG引起的活性氧和丙二醛水平的增加以及足细胞中超氧化物歧化酶活性的降低被Brg-1的过表达所逆转。Brg-1过表达终止了HG诱导的纤连蛋白，IV型胶原，转化生长因子β1和结缔组织生长因子的产生。此外，在HG刺激的足细胞中，Brg-1过表达激活了Akt依赖性核因子E2相关因子2（Nrf2）/抗氧化反应元件（ARE）信号。然而，抑制Akt途径或Nrf2沉默抵消了Brg-1在HG刺激的足细胞中的保护作用。总之，Brg-1过表达通过激活足细胞中依赖Akt的Nrf2 / ARE信号来抑制HG诱导的氧化应激和细胞外基质积累。