AKT inhibitor delays STZ-induced diabetic nephropathy by blocking EndoMT transformation – Research

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.