Astragalus polysaccharide (APS) reduced fasting blood glucose, blood urea nitrogen, and serum creatinine in a rat model.
APS administration decreased renal injury markers, including blood urea nitrogen and serum creatinine levels.
Inflammatory cytokines IL-1β, IL-6, and MCP-1 levels were significantly reduced following APS treatment.
Inhibition of the TLR4/NF-κB signaling pathway was observed in the diabetic nephropathy model after APS administration.
In vitro studies showed that APS alleviated inflammatory responses and podocyte proliferation induced by high glucose.
Simplified
BACKGROUND: (DN), as a chronic inflammatory complication of diabetes, is characterized by hyperglycemia, albuminuria and edema, which ultimately becomes the leading cause of end-stage renal disease (ESRD). Astragalus polysaccharide (APS), extracted from the, was widely used in the treatment of diabetes mellitus. However, the functional roles of APS ameliorate inflammatory responses in DN, which remain poorly understood. Therefore, the purpose of this study was to explore the molecular mechanism of APS on DN in vivo and vitro models. Astragalus membranaceus
METHODS: We explored the beneficial effects of APS in streptozotocin (STZ)-induced DN rat model and high glucose (HG)-treated glomerular podocyte model. The fasting blood glucose (FBG) and ratio of kidney weight to body weight were measured after 4 weeks of APS treatment. The renal injury parameters containing serum creatinine (Scr), blood urea nitrogen (BUN) and 24 h urinary protein were evaluated. The renal pathological examination was observed by hematoxylin-eosin (HE) staining. The levels of IL-1β, IL-6 and MCP-1 were evaluated by ELISA assay. The proliferation of podocytes was determined using CCK-8 assay and flow cytometry. qRT-PCR and Western blot analysis were performed to determine the amounts of TLR4/NF-κB-related gene expression.
RESULTS: Our results indicated that APS effectively decreased the levels of FBG, BUN, Scr and renal pathological damage when compared with STZ-induced DN model group. Additionally, APS significantly ameliorated renal injury by reducing inflammatory cytokines IL-1β, IL-6, MCP-1 expression and inhibiting the activity in DN rats. Consistent with the results in vitro, the HG-induced inflammatory response and proliferation of glomerular podocytes were also alleviated through APS administration.
CONCLUSION: We found that APS ameliorated DN renal injury, and the mechanisms perhaps related to relieving inflammatory responses and attenuating the TLR4/NF-κB signaling pathway.
Key numbers
11.7 mmol/L
Decrease in Fasting Blood Glucose
Blood glucose levels above this threshold indicate successful modeling.
Scr
Decrease in Serum Creatinine
Serum creatinine is a key marker for renal injury in .
BUN
Decrease in Blood Urea Nitrogen
Blood urea nitrogen is another important indicator of kidney function.
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