ArticleFood science & nutrition2024
Epigallocatechin-3-Gallate Ameliorates Diabetic Kidney Disease by Inhibiting the TXNIP/NLRP3/IL-1β Signaling Pathway.
Article in Food science & nutrition, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers, 1 of them a synthesis that pooled it.
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Who cites it
8 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Lipid Peroxidation in Diabetic Kidney Disease: Mechanism and Natural Solution.International journal of molecular sciences · 2025Pooled it
- Epigallocatechin-3-gallate attenuates oxidative stress and apoptosis in podocytes of focal segmental glomerulosclerosis.Renal failure · 2026Article
- An Integrated Therapeutic Strategy for Cardiorenal Syndrome to Target Oxidative Stress, Inflammation, and Fibrosis.Reviews in cardiovascular medicine · 2026Review
- Use of Small Organic Molecules to Improve Pancreatic Beta Cell Resilience to IAPP-Induced Proteotoxic Stress.International journal of molecular sciences · 2026Review
- Review
- Systematic evaluation and comparison of theCurrent research in food science · 2026Article
- The Inflammatory Cell Death in Diabetic Kidney Disease: Integrating Multifactorial Mechanisms into Novel Therapeutics.International journal of molecular sciences · 2025Review
- Deciphering the Genetic Association Between the FODMAP Diet and Recurring Oral Aphthae-The Mediating Role of Ferroptosis.Food science & nutrition · 2025Article
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8 authors.
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Abstract
Recent research indicates that the activation of the NLRP3 inflammasome is crucial in the development of diabetic kidney disease (DKD). Epigallocatechin-3-gallate (EGCG), the predominant catechin in green tea, has been noted for its anti-inflammatory properties in DKD. However, the specific mechanisms are not yet fully understood. In this study, our objective was to explore the effects of EGCG on podocytes and in diabetic kidney disease (DKD) mice and investigate how EGCG modulates the TXNIP/NLRP3/IL-1β signaling pathway in DKD, both in podocytes and animal models. In vitro, we co-cultured podocytes with EGCG and detected the viability, apoptosis, inflammation and the TXNIP/NLRP3/IL-1β signaling pathway. In vivo, DKD mice were given EGCG via oral gavage, followed by evaluations of renal function, inflammation, and the aforementioned signaling pathway. Our findings revealed that oxidative stress, inflammatory cytokines, and the TXNIP/NLRP3/IL-1β pathway were upregulated in podocytes exposed to high glucose (HG) and in the kidneys of DKD mice. However, EGCG treatment reduced the expression of the NLRP3 inflammasome and its associated proteins, including TXNIP, ASC, caspase-1, and IL-1β, as well as the levels of ROS and inflammatory factors such as TNF-α, IL-6, and IL-18. Furthermore, in vivo, EGCG improved kidney function, reduced albuminuria and body weight, and alleviated renal pathological damage. In summary, our study suggests that EGCG mitigates inflammation in podocytes and DKD through the TXNIP/NLRP3/IL-1β signaling pathway, indicating potential benefits of EGCG or green tea in managing DKD.
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