Abstract
Background Diabetic nephropathy (DN), a complication of diabetes, is the result of high glucose-induced pathological changes in podocytes, such as epithelial-mesenchymal transition (EMT). Autophagy is an important mechanism of podocyte repair. Ginsenoside Rg1, the active ingredient of ginseng extract, has antifibrotic and proautophagic effects. Therefore, we hypothesized that ginsenoside Rg1 can reverse podocyte EMT via autophagy and alleviate DN. Aim This study aimed to investigate the effect of ginsenoside Rg1 on DN rats and high glucose-induced podocyte EMT by regulating the AKT/GSK3β/β/Methods Diabetic rats induced by STZ injection were treated with 50 mg/kg ginsenoside Rg1 for 8 weeks, and the renal functional, metabolic, and histopathological indices were evaluated. DN was simulated in vitro by exposing podocytes to high glucose levels and treated with ginsenoside Rg1. The expression of EMT and autophagy-related markers was analyzed in vivo and in vitro by exposing podocytes to high glucose levels and treated with ginsenoside Rg1. The expression of EMT and autophagy-related markers was analyzed Results Ginsenoside Rg1 significantly alleviated renal fibrosis and podocyte EMT in diabetic rats, and podocytes exposed to high glucose levels, which was abolished by the autophagy inhibitor 3-MA. Furthermore, ginsenoside Rg1 regulated the AKT/GSK3 β/β/Conclusion Ginsenoside Rg1 alleviated podocyte EMT by enhancing AKT/GSK3β/β-catenin pathway-mediated autophagy, indicating its therapeutic potential for DN and other glomerular diseases.β/β/
Highlights
Diabetic nephropathy (DN) is a serious microvascular complication of diabetes [1] and a common cause of chronic renal failure. e prominent pathological feature of DN is glomerular sclerosis, which manifests as proteinuria in the early stages of the disease, and is an important indicator of its severity [2]. e mechanistic basis of proteinuria in DN is podocyte injury, which is the result of apoptosis and the subsequent decrease in their number and density [3, 4]
Compared to the control animals, all indices of renal function-renal weight/body weight ratio and the levels of serum creatinine, urea nitrogen, urinary creatinine, and urinary microalbumin were significantly increased in the DN group
Ginsenoside Rg1 improved the above parameters in the DN rats (see Figures 2(a)–2(d)), indicating an ameliorative effect on renal metabolism and proteinuria
Summary
Diabetic nephropathy (DN) is a serious microvascular complication of diabetes [1] and a common cause of chronic renal failure. e prominent pathological feature of DN is glomerular sclerosis, which manifests as proteinuria in the early stages of the disease, and is an important indicator of its severity [2]. e mechanistic basis of proteinuria in DN is podocyte injury, which is the result of apoptosis and the subsequent decrease in their number and density [3, 4]. An alternative possibility is high glucose-induced epithelial-mesenchymal transition (EMT) of the podocytes, which disrupts their structure and function, and damages the integrity of the glomerular filtration barrier leading to proteinuria, glomerular sclerosis, and renal dysfunction. Diabetic nephropathy (DN), a complication of diabetes, is the result of high glucose-induced pathological changes in podocytes, such as epithelial-mesenchymal transition (EMT). Aim. is study aimed to investigate the effect of ginsenoside Rg1 on DN rats and high glucose-induced podocyte EMT by regulating the AKT/GSK3β/β-catenin pathway by restoring autophagy activity. Ginsenoside Rg1 significantly alleviated renal fibrosis and podocyte EMT in diabetic rats, and podocytes exposed to high glucose levels, which was abolished by the autophagy inhibitor 3-MA. Ginsenoside Rg1 alleviated podocyte EMT by enhancing AKT/GSK3β/β-catenin pathwaymediated autophagy, indicating its therapeutic potential for DN and other glomerular diseases
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