ArticleFrontiers in pharmacology2025
Ophiopogonin D improves pancreatic islet cell dedifferentiation to treat diabetes by regulating the GRP78/ROS/PDX1 signaling pathway.
Article in Frontiers in pharmacology, 2025. 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.
- Research Progress and Prospects of Saponins in the Treatment of NAFLD: A Narrative Review.Molecules (Basel, Switzerland) · 2025Review
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11 authors.
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Abstract
Introduction: The incidence of diabetes is rising annually, significantly impacting public health and imposing a substantial economic burden on society. Ophiopogonin D (Op D) exhibits certain hypoglycemic effects; however, its mechanisms remain unclear. Methods: β-cell dedifferentiation, distinct from β-cell apoptosis, is a pathogenic mechanism we aim to explore regarding Op D's regulatory effects. We established an animal model of β-cell dedifferentiation to assess Op D's impact on glucose tolerance, blood glucose levels, and insulin secretion. We employed immunohistochemistry and immunofluorescence to analyze the expression levels of dedifferentiation-related proteins. Additionally, we created an Results: Results indicated that Op D reduced blood glucose levels, improved glucose tolerance, enhanced insulin secretion, mitigated pancreatic atrophy, and increased PDX1 and FOXO1 expression levels. Furthermore, Op D inhibited ER stress, decreased GRP78 expression, reduced NGN3 levels, elevated PDX1, NKX6.1, and MAFA expression, and decreased oxidative stress-related products (ROS, MDA) while increasing SOD and GSH levels. Discussion: These findings demonstrate that Op D can improve β-cell dedifferentiation by modulating the GRP78/ROS/PDX1 pathway to inhibit ER stress.
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