ArticleDigestive diseases and sciences2024
Glycyrrhizin Ameliorates Cardiac Injury in Rats with Severe Acute Pancreatitis by Inhibiting Ferroptosis via the Keap1/Nrf2/HO-1 Pathway.
Article in Digestive diseases and sciences, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed.
- Beyond Supportive Care: Mitochondria as a Strategic Therapeutic Avenue in Acute Pancreatitis.Digestive diseases and sciences · 2026Review
- Cell death and its interaction with mitochondrial dysfunction in pathogenesis of acute pancreatitis: a comprehensive review.Apoptosis : an international journal on programmed cell death · 2026Review
- 3D vascular mapping reveals multi-organ injury following severe acute pancreatitis.Theranostics · 2026Article
- Article
- Ferroptosis in acinar cells of traumatic pancreatitis: implications for predictive, preventive, and personalized approaches in intra-abdominal infection management.The EPMA journal · 2025Article
- Protective Effect of Hordenine on Concanavalin A-Induced Hepatic Injury.Journal of inflammation research · 2025Article
- An overview of current research on the modulation of NLRP3 inflammasome by traditional Chinese medicine to combat acute pancreatitis.Frontiers in molecular biosciences · 2025Review
- Targeting the programmed cell death signaling mechanism with natural products for the treatment of acute pancreatitis: a review.Frontiers in pharmacology · 2025Review
- Cardiac complications in acute pancreatitis: an under-diagnosed clinical concern.World journal of emergency medicine · 2025Article
- Mechanism of minocycline activating Nrf2/Hmox1 pathway to prevent ferroptosis and alleviate acute compartment syndrome.Journal of orthopaedic surgery and research · 2024Article
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Authors and funding
8 authors.
Funding
Abstract
backgroundSevere acute pancreatitis (SAP) is a potential fatal gastrointestinal disease that is usually complicated by myocardial injury and dysfunction. Due to the lack of understanding of the mechanism of SAP-associated cardiac injury (SACI), there is still no complete treatment.
aimsTo explore the alleviative effect and anti-ferroptosis mechanism against SACI of glycyrrhizin (GL), an inhibitor of oxidative stress.
methodsThe SAP model was established by perfusing 5% sodium taurocholate into biliopancreatic duct in rats. H&E staining and serum assays were used to assess the injury changes of pancreas and heart. Echocardiography was used to evaluate the cardiac function. Transmission electron microscopy (TEM) and oxidative stress assays were used to investigate the ferroptosis-related morphological and biochemical changes. Western blot and immunofluorescence were performed to analyzed the expression of ferroptosis-related proteins.
resultsSignificant myocardial impairment was found in SAP rats according to increased histopathological scores, serum creatine kinase-MB (CK-MB) and cardiac troponin-I (cTnI) levels, and a decreased fractional shortening and ejection fraction. The decreased mitochondrial cristae and significant expression changes of ferroptosis-related proteins confirmed the presence of ferroptosis in SACI. GL treatment attenuated above-mentioned cardiac tissues damage by inhibiting ferroptosis via restoring the expression of Nrf2 and HO-1 in vivo and in vitro. Treating with ML385 (a Nrf2 inhibitor) or transfecting with siRNA-Nrf2 reversed the protective effect of GL.
conclusionsOur findings demonstrate the involvement of ferroptosis in SACI and suggest a potential role for GL in the treatment of SACI by supressing ferroptosis via Keap1/Nrf2/HO-1 pathway.
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38753240What Socratic holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.