ArticleMolecular and cellular biochemistry2019
Bone marrow-derived mesenchymal stem cells ameliorate severe acute pancreatitis by inhibiting necroptosis in rats.
Article in Molecular and cellular biochemistry, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 18 citations in OpenAlex.
- 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
- The role and interplay among Autophagy, Apoptosis, and ferroptosis in acute pancreatitis: mechanisms and therapeutic approaches.Molecular biology reports · 2025Review
- Review
- Bone marrow-derived mesenchymal stem cells ameliorate severe acute pancreatitis by inhibiting oxidative stress in rats.Molecular and cellular biochemistry · 2022Article
- Understanding Necroptosis in Pancreatic Diseases.Biomolecules · 2022Review
- Targeted Therapy for Inflammatory Diseases with Mesenchymal Stem Cells and Their Derived Exosomes: From Basic to Clinics.International journal of nanomedicine · 2022Review
- Evidence of Stem Cells Mobilization in the Blood of Patients with Pancreatitis: A Potential Link with Disease Severity.Stem cells international · 2022Article
- Optimal concentration of necrostatin-1 for protecting against hippocampal neuronal damage in mice with status epilepticus.Neural regeneration research · 2020Article
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Authors and funding
8 authors at 5 institutions in 1 country.
Funding
Abstract
The treatment and prognosis for severe acute pancreatitis (SAP) is currently unsatisfactory showing a high incidence of morbidity and mortality. Here, we investigated the effect of bone marrow-derived mesenchymal stem cells (BMSCs) on SAP in rats and explored the possible mechanisms. The common bile duct of each model rat was occluded at the liver hilum, and the induction of SAP was achieved by retrograde perfusion of 3% sodium taurocholate (NaT). Prepared BMSCs were intravenously injected via the tail vein. Pancreatic acinar cells (PACs) were isolated from rat pancreas, and induced by TNF-α. In the present study, we found that necroptosis was activated in NaT-induced acute-necrotized pancreatitis, and transplanted BMSCs could inhibit necroptosis, repair pancreatic injury, and reduce systemic inflammatory response. In addition, necrostatin-1 (Nec-1), as the inhibitor of receptor-interacting protein kinase 1 (RIPK1), could also reduce SAP to some extent. Besides, we detected that BMSCs could also promote regeneration of damaged pancreatic tissues. Furthermore, in vitro, we also investigated that BMSCs could suppress TNF-α-induced necroptosis and improve the viability of PACs. In addition, Nec-1 and knockdown of receptor-interacting protein kinase 3 (RIPK3) or mixed lineage kinase domain-like protein (MLKL) could also inhibit necrosis of PACs induced by TNF-α. BMSCs ameliorated SAP and reduced injury of PACs by suppressing the activation of the necroptosis signaling pathway.
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