Abstract
ObjectiveTo investigate the effect of baicalin on diabetic nephropathy (DN) rats and podocytes and its mechanism.MethodsThe rat models with DN were established by high-fat and high-sugar diet and intraperitoneal injection of streptozotocin. The fasting blood glucose (FBG) and weight of rats in each group were measured at 0, 1, 2, 3, and 4 weeks. Their biochemical indicators, expression of inflammatory, and antioxidant factors were measured using an automatic biochemical analyzer together with ELISA. Hematoxylin–eosin staining and periodic acid-schiff staining were used to observe the morphological changes in the kidneys of rats in each group. Finally, the expressions of related molecules and PI3K/Akt/mTOR signaling pathway proteins in renal tissues and podocytes were examined by qRT-PCR and Western blot.ResultsCompared with the DN group, the FBG and weight, serum creatinine, blood urea nitrogen, total cholesterol, triacylglycerol, microalbumin, and albumin/creatinine ratio were all significantly decreased in the Baicalin treatment groups in a concentration-dependent manner. The levels of inflammatory factors in kidney tissue and podocytes were decreased. In addition, the activities of lactate dehydrogenase and malondialdehyde in tissue were decreased, while the superoxide dismutase was increased. The pathological sections showed that glomerular atrophy and glomerular basement membrane thickening caused by hyperglycemia were improved in the Baicalin treatment groups. Meanwhile, baicalin inhibited the downregulation of Nephrin and Podocin expressions and upregulation of Desmin expression caused by DN, and inhibited the expressions of p-PI3K, p-Akt, and p-mTOR proteins.ConclusionBaicalin slows down podocyte injury caused by DN by inhibiting the activity of PI3K/Akt/mTOR signaling pathway.
Highlights
Diabetic nephropathy (DN) is a disease in which diabetes mellitus (DM) induces vascular lesions, promoting glomerulosclerosis [1]
The total RNA was reverse transcribed into cDNA using MLV reverse transcriptase. qPCR was performed in the detection system of SYBR Green Master Mix (Promega, USA)
RIPA lysis buffer was added to the podocytes and centrifuged at 12,000 rpm for 30 min at 4°C; the supernatant was taken as total protein
Summary
Diabetic nephropathy (DN) is a disease in which diabetes mellitus (DM) induces vascular lesions, promoting glomerulosclerosis [1]. DN is characterized by diffuse thickening of the glomerular basement membrane (GBM), proliferation and dilatation of the mesangial matrix, and other morphological changes, inducing renal dysfunction. It has been shown that the persistent hyperglycemic state in the peripheral blood of DM patients changes hemodynamics and increases oxidative stress in the body, causing severe injury to local renal cells such as glomerular capillary endothelial cells and podocytes [5]. Podocytes, as terminally differentiated cells, are the important functional cells in the renal glomerulus. Because of the terminal differentiation, podocytes cannot regenerate once subjected to destruction [6]. Hyperglycemia destroys the GBM, resulting in podocyte hypertrophy and detachment. Podocyte content in urine was proposed to be used as a marker to determine the
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