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Updated: Feb 2, 2026

Mechanism of Kemeng Fang's Inhibition of Podocyte Apoptosis in Rats with Membranous Nephropathy through the PI3K/AKT Signaling Pathway
Published on: August 23, 2024
AKT inhibitor delays STZ-induced diabetic nephropathy by blocking EndoMT transformation
Yue Chen1, Yuanjing Li2, Xing Wen3
1Department of Oncology, Chongqing University Jiangjin Hospital, Chongqing, China.
Background:
Diabetic nephropathy (DN) is one of the most common and serious microvascular complications of diabetes, and a leading cause of end-stage renal disease.
Objective:
To investigate whether an AKT inhibitor can regulate EndoMT and participate in the pathogenesis of DN.
Methods:
Thirty Wistar rats were randomly divided into three groups: control, DN model, and AKT inhibitor VIII treatment (20 µM, administered daily via intravenous injection for 4 weeks). Levels of serum creatinine (Scr), blood urea nitrogen (BUN), urinary albumin (UAlb), reactive oxygen species (ROS), superoxide dismutase (SOD), inflammatory factors (IL-6, IL-1β), and the expression of EndoMT-related markers (VE-cadherin, CD31, α-SMA, collagen I) were measured.
Results:
Compared with the DN group, the AKT inhibitor significantly decreased the levels of Scr, BUN, UAlb, ROS, IL-6, IL-1β, TGF-β1, α-SMA, Collagen I and p-AKT (P<0.05), while it increased SOD activity and the expression of VE-Cadherin and CD31.
Conclusion:
The AKT inhibitor may delay the progression of diabetic nephropathy by inhibiting EndoMT, alleviating inflammation, and reducing oxidative stress.
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