ArticleBritish journal of pharmacology2018
Dihydrodiosgenin protects against experimental acute pancreatitis and associated lung injury through mitochondrial protection and PI3Kγ/Akt inhibition.
Article in British journal of pharmacology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 39 citations in OpenAlex.
- Beyond Supportive Care: Mitochondria as a Strategic Therapeutic Avenue in Acute Pancreatitis.Digestive diseases and sciences · 2026Review
- Innovative strategies for anti-fibrotic drugs discovery from traditional Chinese medicine.Chinese herbal medicines · 2026Review
- Mitochondrial dysfunction as a bridge to pathology in acute pancreatitis: From molecular insights to novel therapeutic strategies.World journal of gastroenterology · 2025Review
- Review
- Bioactive Metabolites ofFoods (Basel, Switzerland) · 2025Review
- Immunoengineered mitochondria for efficient therapy of acute organ injuries via modulation of inflammation and cell repair.Science advances · 2025Article
- From micro to macro, nanotechnology demystifies acute pancreatitis: a new generation of treatment options emerges.Journal of nanobiotechnology · 2025Review
- CPT1A mediated preservation of mitochondrial inhibits pyroptosis in pancreatic acinar cells.Frontiers in cell and developmental biology · 2025Article
- Blocking TRPM4 alleviates pancreatic acinar cell damage via an NMDA receptor-dependent pathway in acute pancreatitis.Theranostics · 2025Article
- Computational biology-based study of the molecular mechanism of spermidine amelioration of acute pancreatitis.Molecular diversity · 2024Article
- Network pharmacology and in vitro experimental verification unveil glycyrrhizin from glycyrrhiza glabra alleviates acute pancreatitis via modulation of MAPK and STAT3 signaling pathways.BMC complementary medicine and therapies · 2024Article
- Mitochondrial dysfunction in pancreatic acinar cells: mechanisms and therapeutic strategies in acute pancreatitis.Frontiers in immunology · 2024Review
- Hesperidin Alleviates Acute Necrotizing Pancreatitis by Activating SIRT1 - Molecular Docking, Molecular Dynamics Simulation, and Experimental Validation.Combinatorial chemistry & high throughput screening · 2024Article
- Calcium/P53/Ninjurin 1 Signaling Mediates Plasma Membrane Rupture of Acinar Cells in Severe Acute Pancreatitis.International journal of molecular sciences · 2023Article
- Review
- The Rabep1-Mediated Endocytosis and Activation of Trypsinogen to Promote Pancreatic Stellate Cell Activation.Biomolecules · 2022Article
- Article
- Protective effects of the notoginsenoside R1 on acute lung injury by regulating the miR-128-2-5p/Tollip signaling pathway in rats with severe acute pancreatitis.Innate immunity · 2022Article
- Vitamin BOxidative medicine and cellular longevity · 2021Article
- Natural product derived phytochemicals in managing acute lung injury by multiple mechanisms.Pharmacological research · 2021Review
Corrections and comments
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Authors and funding
11 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
background and purposeAcute pancreatitis (AP) is a painful and distressing disorder of the exocrine pancreas with no specific treatment. Diosgenyl saponins extracted from from Dioscorea zingiberensis C. H. Wright have been reported to protect against experimental models of AP. Diosgenin, or its derivatives are anti-inflammatory in various conditions. However, the effects of diosgenin and its spiroacetal ring opened analogue, dihydrodiosgenin (Dydio), on AP have not been determined. EXPERIMENTAL APPROACH: Effects of diosgenin and Dydio on sodium taurocholate hydrate (Tauro)-induced necrosis were tested, using freshly isolated murine pancreatic acinar cells. Effects of Dydio on mitochondrial dysfunction in response to Tauro, cholecystokinin-8 and palmitoleic acid ethyl ester were also assessed. Dydio (5 or 10 mg·kg KEY
resultsDydio inhibited Tauro-induced activation of the necrotic cell death pathway and prevented pancreatitis stimuli-induced mitochondrial dysfunction. Therapeutic administration of Dydio ameliorated biochemical and histopathological responses in all three models of AP through pancreatic mitochondrial protection and PI3Kγ/Akt inactivation. Moreover, Dydio improved pancreatitis-associated acute lung injury through preventing excessive inflammatory responses. CONCLUSION AND IMPLICATIONS: These data provide in vitro and in vivo mechanistic evidence that the diosgenin analogue, Dydio could be potential treatment for AP. Further medicinal optimization of diosgenin and its analogue might be a useful strategy for identifying lead candidates for inflammatory diseases.
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