ArticleDiabetes, metabolic syndrome and obesity : targets and therapy2022
Sacubitril/Valsartan Improves Progression of Early Diabetic Nephropathy in Rats Through Inhibition of NLRP3 Inflammasome Pathway.
Article in Diabetes, metabolic syndrome and obesity : targets and therapy, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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5 citing papers in PubMed, 9 citations in OpenAlex.
- Azilsartan Ameliorates Diabetic Kidney Disease Through Modulation of Inflammation, Pyroptosis, and Mitochondrial Dysfunction.Journal of diabetes research · 2026Article
- Molecular mechanisms underlying cyclophosphamide-induced ovarian injury and protective strategies.Naunyn-Schmiedeberg's archives of pharmacology · 2026Review
- Ameliorative impact of sacubitril/valsartan on paraquat-induced acute lung injury: role of Nrf2 and TLR4/NF-κB signaling pathway.Naunyn-Schmiedeberg's archives of pharmacology · 2025Article
- BOLD MRI to Evaluate the Effects of Sacubitril/Valsartan on Renal Protection in Type 2 Diabetics.Diabetes, metabolic syndrome and obesity : targets and therapy · 2025Article
- Article
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6 authors at 2 institutions in 1 country.
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Abstract
Purpose: Diabetic nephropathy (DN), a global disease, is the leading cause of end-stage renal disease. There is a lack of specific treatment for this disease, and early intervention in disease progression is essential. In this paper, we used a rat model of early diabetic nephropathy to explore the therapeutic mechanism of sacubitril/valsartan in rats with early diabetic nephropathy. Materials and Methods: Rats were grouped into 1 normal group; 2. Model group (DN group): STZ (45 mg/kg/d) induced early diabetic nephropathy rats; 3. Sac group: DN rats + Sac group (orally, 60 mg/kg/d) for 6 weeks. After 6 weeks, the levels of serum albumin (ALB), glucose (GLU), creatinine (Cr), urea nitrogen (BUN) and 24-h urinary protein excretion were measured. In renal tissue homogenates, NLRP3 inflammasome, proinflammatory factors IL1-β and TNF-α, oxidative stress MDA and pro-fibrotic cytokine TGF-β1 were performed. Histological analysis of kidneys by hematoxylin and eosin (HE), PAS and Masson trichrome staining. Results: 1. Sacubitril/valsartan (Sac) significantly improved renal hypertrophy, proteinuria and serum albumin levels in rats with early diabetic nephropathy (P < 0.001), and decreased GLU, Scr (P<0.001), and BUN levels (P < 0.01).2. Light microscopy of renal tissues showed glomerular hypertrophy and interstitial inflammatory cell infiltration, and mean glomerular area (MGA) and mean glomerular volume (MGV) were crucially increased in early diabetic nephropathy (P < 0.001), and the Sac group showed reduced renal pathology and improved MGA and MGV (P < 0.001).3. Kidney tissue homogenate levels of NLRP3, Caspase-1, IL1-β, TNF-α, MDA and TGF-β1 were critically, increased in DN rats (P < 0.001), and SOD was significantly decreased. All these indicators above were improved after treatment (P < 0.0001). Conclusion: Nlrp3-inflammasome promote progression of diabetic nephropathy through inflammation, fibrosis and oxidative stress; sacubitril/valsartan ameliorated early diabetes-induced renal damage by inhibiting NLRP3 pathway activation.
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