ArticleBiomedicines2022
The Role of NF-κB and Bax/Bcl-2/Caspase-3 Signaling Pathways in the Protective Effects of Sacubitril/Valsartan (Entresto) against HFD/STZ-Induced Diabetic Kidney Disease.
Article in Biomedicines, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed, 32 citations in OpenAlex.
- Sacubitril/valsartan attenuates renal injury caused by cecal ligation and puncture via TLR4/NFκB/NLRP3 inhibition and reduced oxidative stress and apoptosis in rats.Scientific reports · 2026Article
- Investigation of Protective Effects of Carvacrol and Hesperidin in Rats with Streptozotocin-Induced Diabetic Nephropathy.Life (Basel, Switzerland) · 2026Article
- The effects of sacubitril/valsartan compared to valsartan in experimentally induced chronic kidney disease.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- Multiomics Integration Analysis Reveals the Regulatory Mechanisms of Efferocytosis in Diabetic Kidney Disease.Inflammation · 2026Article
- Analysis of high glucose injury using human induced pluripotent stem cell-derived kidney organoids.BMC nephrology · 2026Article
- Sacubitril/valsartan mitigates cisplatin-induced liver injury through modulation of oxidative stress, Caspase-3 activity, and RXR-α signaling in experimental rats.Frontiers in pharmacology · 2026Article
- Azilsartan Ameliorates Diabetic Kidney Disease Through Modulation of Inflammation, Pyroptosis, and Mitochondrial Dysfunction.Journal of diabetes research · 2026Article
- Beyond Organ Boundaries: Molecular Mechanisms of Hepatic Encephalopathy and Parkinson's Disease from the Perspective of the Gut-Liver-Brain Axis.Research (Washington, D.C.) · 2026Review
- Effects of Carvacrol on Oxidative Stress and Fibrosis in Streptozotocin-Induced Diabetic Nephropathy: Histological, Gene Expression, and Biochemical Insights.International journal of molecular sciences · 2025Article
- Integrative analysis of mitochondrial and immune pathways in diabetic kidney disease: identification of AASS and CASP3 as key predictors and therapeutic targets.Renal failure · 2025Article
- Mitochondrial dysfunction: the hidden catalyst in chronic kidney disease progression.Renal failure · 2025Review
- Tectoridin modulates intertwined molecular pathways in metabolic syndrome: insights from network pharmacology, molecular docking, and in vivo studies.Inflammopharmacology · 2025Article
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- PCSK9 Inhibitors: A Potential Priority Choice for Lipid Management in Patients with Diabetic Kidney Disease.Drugs · 2025Review
- 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
- Programmed Cell Death in Diabetic Kidney Disease: Mechanisms and Therapeutic Targeting.Journal of inflammation research · 2025Review
- Rosmarinic acid attenuated inflammation and apoptosis in folic acid-induced renal injury: Role of FoxO3/ NFκB pathway.Iranian journal of basic medical sciences · 2025Article
- Article
- Capsaicin reduces blood glucose and prevents prostate growth by regulating androgen, RAGE/IGF-1/Akt, TGF-β/Smad signalling pathway and reversing epithelial-mesenchymal transition in streptozotocin-induced diabetic mice.Naunyn-Schmiedeberg's archives of pharmacology · 2024Article
- Article
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3 authors at 1 institution in 1 country.
Funding
Abstract
LCZ696 (valsartan/sacubitril) has the potential to slow the progression of diabetic kidney disease (DKD) according to previous reports. However, the renoprotective mechanism underlying LCZ696 remains unknown. This study aimed to investigate the therapeutic potential and underlying mechanism of LCZ696 in DKD in a type 2 diabetic (T2D) rat model. This model was established in this experiment by feeding a high-fat diet (HFD) for six weeks with a single dose of streptozotocin (STZ, 30 mg/kg body weight). Valsartan or LCZ696 was orally administered to T2D animals for eight weeks. HFD/STZ rats showed hyperglycemia, impaired insulin secretion, significant increases in urea, creatinine, cytokines, nuclear factor kappa B (NF-κB), oxidative stress, caspase-3 activity, glomerular and tubular damage, glomerulsclerosis, Bax and caspese-3 expressions along with a significant decline in IL-10, antioxidant markers, and Bcl-2 expression. The administration of LCZ696 to diabetic rats reduced the serum concentrations of glucose, urea, and creatinine. In addition, ELISA results demonstrated that diabetic rats treated with LCZ696 exhibited a reduction in inflammatory (IL-1β, TNF-α, IL-6) and an increase in anti-inflammatory (IL-10) cytokine levels. In addition, a notable decrease in NF-κB and caspase-3 activity was observed. At the level of renal tissue homogenate, diabetic animals treated with LCZ696 demonstrated clear restorations in GSH content and other antioxidant enzyme levels, in addition to a significant decrease in TBARS levels. In addition, LCZ696 inhibited the expression of the Bax and cleaved caspase-3 proteins and enhanced the expression of the Bcl-2 protein. Improvements in histopathological changes in kidney tissues confirmed and significantly supported these biochemical findings. In summary, LCZ696 alleviated DKD with possible mechanisms including inhibition of inflammation and apoptosis.
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