ArticleMolecular and cellular biochemistry2026
Innovative valsartan-loaded self-nanoemulsifying drug delivery system combat liver inflammation and oxidative stress in streptozotocin-induced diabetic rats.
Article in Molecular and cellular biochemistry, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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1 citing paper in PubMed.
- EPA-loaded silica nanoemulsions attenuate DEN-induced hepatic fibroinflammation by modulating homocysteine, PKCα/NF-κB, and Nrf2 signaling.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
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8 authors.
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Abstract
Diabetes-induced liver damage is a significant complication of hyperglycemia, which results in oxidative stress, inflammation, and fibrosis. Conventional treatment strategies remain limited, necessitating novel therapeutic approaches. This study evaluates the hepatoprotective effects of valsartan-loaded self-nanoemulsifying drug delivery system (SNEDDS) in streptozotocin (STZ)-induced hyperglycemic rats, focusing on oxidative stress modulation, suppression of inflammatory cytokines, and metabolic regulation. Male Sprague-Dawley rats were divided into six groups: control, STZ-induced diabetic model, and treatment diabetic groups receiving valsartan (Val) or valsartan/hydrochlorothiazide (Val/HCT) in either SNEDDS-loaded liquisolid tablets or directly compressed tablets. Liver function, oxidative stress biomarkers, lipid profiles, histopathological changes, and gene expression levels of NF-κB, TGF-β, and Nrf2 were assessed. Val and Val/HCT-loaded-SNEDDS significantly reduced fasting blood glucose to ~ 95 mg/dl, serum ALT levels (34-50%), and pro-inflammatory cytokines (NF-κB and IL-1) (21% and 40%, respectively). They also enhanced antioxidant defenses by increasing hepatic glutathione levels (34-39%) while reducing malondialdehyde (36-39%) and nitric oxide (50%). Histopathological analysis confirmed improved liver architecture with diminished inflammatory cell infiltration and fibrosis. Gene expression analysis revealed a downregulation of TGF-β and NF-κB, alongside upregulation of Nrf2, indicating reduced fibrogenesis and an oxidative stress response. In conclusion, Val-loaded SNEDDS effectively mitigates STZ-induced hepatotoxicity. This hepatoprotective effect is due to blocking the angiotensin II type 1 receptor (AT1R), leading to inhibition of TGF-β and other TGF-β-mediated inflammatory markers, such as NF-κB and IL-1. This nanoformulation offers a promising therapeutic strategy for diabetes-associated liver injury and warrants further investigation for clinical applications.
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