ArticleGenes & genomics2023
Reduction of high glucose-induced oxidative injury in human retinal pigment epithelial cells by sarsasapogenin through inhibition of ROS generation and inactivation of NF-κB/NLRP3 inflammasome pathway.
Article in Genes & genomics, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 10 citations in OpenAlex.
- Mechanistic insights into natural product-driven modulation of NLRP3-inflammasome signalling in metabolic syndrome.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026Review
- Protective role of zingerone against high glucose-Induced retinal pigment epithelial cell damage through modulation of the TRPM2 channel pathway.Molecular biology reports · 2026Article
- Role of the NLRP3 inflammasome in diabetes and its complications (Review).Molecular medicine reports · 2025Review
- Sarsasapogenin protects hair cells from cisplatin-induced ototoxicity by attenuating apoptosis and ferroptosis via alleviating oxidative stress.Frontiers in pharmacology · 2025Article
- Fenofibrate mitigates the dysfunction of high glucose-driven human retinal microvascular endothelial cells by suppressing NLRP3 inflammasome.International journal of ophthalmology · 2025Article
- Research progress of diabetic retinopathy and gut microecology.Frontiers in microbiology · 2023Review
- Preliminary evaluation of the antiglycoxidant activity of verapamil using variousFrontiers in pharmacology · 2023Article
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1 author at 1 institution in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
backgroundHyperglycemia-induced accumulation of reactive oxygen species (ROS) is a major risk factor for diabetic retinopathy (DR). Sarsasapogenin is a natural steroidal saponin that is known to have excellent antidiabetic effects and improve diabetic complications, but its potential efficacy and mechanism for DR are unknown.
objectivesThe current study was designed to explore whether sarsasapogenin inhibits hyperglycemia-induced oxidative stress in human retinal pigment epithelial (RPE) ARPE-19 cells and to elucidate the molecular mechanisms.
methodsTo mimic hyperglycemic conditions, ARPE-19 cells were cultured in medium containing high glucose (HG). The suppressive effects of sarsasapogenin on HG-induced cell viability reduction, apoptosis and ROS production were investigated. In addition, the relevance of the nuclear factor-kappa B (NF-κB)/NOD-like receptor family pyrin domain-containing 3 (NLRP3) inflammasome signaling pathway was explored to investigate the mechanism of antioxidant and anti-inflammatory activity of sarsasapogenin.
resultsSarsasapogenin significantly alleviated cytotoxicity and apoptosis in HG-treated ARPE-19 cells through inhibition of intracellular ROS generation. Sarsasapogenin also effectively attenuated HG-induced excess accumulation of mitochondrial superoxide, reduction of glutathione content, and inactivation of manganese superoxide dismutase and glutathione peroxidase. The HG condition markedly increased the expression and maturation of interleukin (IL)-1β and IL-18 through the activation of the NF-kB signaling pathway, whereas sarsasapogenin reversed these effects. Moreover, although the expression of NLRP3 inflammasome multiprotein complex molecules was increased in ARPE-19 cells cultured under HG conditions, their levels remained similar to the control group in the presence of sarsasapogenin.
conclusionSarsasapogenin could protect RPE cells from HG-induced injury by inhibiting ROS generation and NF-κB/NLRP3 inflammasome pathway, suggesting its potential as a therapeutic agent to improve the symptoms of DR.
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