ArticleJournal of cellular and molecular medicine2016
Lentinan protects pancreatic β cells from STZ-induced damage.
Article in Journal of cellular and molecular medicine, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 57 citations in OpenAlex.
- Revitalizing Pleurotus eryngii polysaccharides: gamma irradiation boosts antidiabetic and antioxidant potential.Bioresources and bioprocessing · 2025Article
- Quercetin prevents rats from type 1 diabetic liver damage by inhibiting TGF-ꞵ/apelin gene expression.Current research in pharmacology and drug discovery · 2024Article
- Rosemarinic acid protects β-cell from STZ-induced cell damage via modulating NF-κβ pathway.Heliyon · 2023Article
- The metabolic and molecular mechanisms of α‑mangostin in cardiometabolic disorders (Review).International journal of molecular medicine · 2022Review
- Lentinan alleviates arsenic-induced hepatotoxicity in mice via downregulation of OX40/IL-17A and activation of Nrf2 signaling.BMC pharmacology & toxicology · 2022Article
- Lentinan Protects against Nonalcoholic Fatty Liver Disease by Reducing Oxidative Stress and Apoptosis via the PPARα Pathway.Metabolites · 2022Article
- Lentinan Enhances the Function of Oxaliplatin on the Esophageal Tumors by Persuading Immunogenic Cell Death.Computational and mathematical methods in medicine · 2022Article
- The Dectin-1 Receptor Signaling Pathway Mediates the Remyelination Effect of Lentinan through Suppression of Neuroinflammation and Conversion of Microglia.Journal of immunology research · 2022Article
- Tat-CIAPIN1 protein prevents against cytokine-induced cytotoxicity in pancreatic RINm5F β-cells.BMB reports · 2021Article
- Adjuvant Therapy With Mushroom Polysaccharides for Diabetic Complications.Frontiers in pharmacology · 2020Review
- Article
- Protective effects of Tat-DJ-1 protein against streptozotocin-induced diabetes in a mice model.BMB reports · 2018Article
- Alpha-Mangostin Improves Insulin Secretion and Protects INS-1 Cells from Streptozotocin-Induced Damage.International journal of molecular sciences · 2018Article
- HX-1171 attenuates pancreatic β-cell apoptosis and hyperglycemia-mediated oxidative stress via Nrf2 activation in streptozotocin-induced diabetic model.Oncotarget · 2018Article
- Metabolomics insights into the modulatory effects of long-term compound polysaccharide intake in high-fat diet-induced obese rats.Nutrition & metabolism · 2018Article
- Selective and sensitive visualization of endogenous nitric oxide in living cells and animals by a Si-rhodamine deoxylactam-based near-infrared fluorescent probe.Chemical science · 2017Article
- Cyclocarya paliurus tea leaves enhances pancreatic β cell preservation through inhibition of apoptosis.Scientific reports · 2017Article
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Pancreatic β-cell death or dysfunction mediated by oxidative stress underlies the development and progression of diabetes mellitus (DM). In this study, we evaluated the effect of lentinan (LNT), an active ingredient purified from the bodies of Lentinus edodes, on pancreatic β-cell apoptosis and dysfunction caused by streptozotocin (STZ) and the possible mechanisms implicated. The rat insulinoma cell line INS-1 were pre-treated with the indicated concentration of LNT for 30 min. and then incubated for 24 hrs with or without 0.5 mM STZ. We found that STZ treatment causes apoptosis of INS-1 cells by enhancement of intracellular reactive oxygen species (ROS) accumulation, inducible nitric oxide synthase (iNOS) expression and nitric oxide release and activation of the c-jun N-terminal kinase (JNK) and p38 mitogen-activated protein kinase (MAPK) signalling pathways. However, LNT significantly increased cell viability and effectively attenuated STZ-induced ROS production, iNOS expression and nitric oxide release and the activation of JNK and p38 MAPK in a dose-dependent manner in vitro. Moreover, LNT dose-dependently prevented STZ-induced inhibition of insulin synthesis by blocking the activation of nuclear factor kappa beta and increasing the level of Pdx-1 in INS-1 cells. Together these findings suggest that LNT could protect against pancreatic β-cell apoptosis and dysfunction caused by STZ and therefore may be a potential pharmacological agent for preventing pancreatic β-cell damage caused by oxidative stress associated with diabetes.
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