Lentinan protects against pancreatic β‐cell failure in chronic ethanol consumption‐induced diabetic mice via enhancing β‐cell antioxidant capacity
Autor: | Xiao Han, Tijun Wu, Lin Wang, Fang Chen, Yixue Shao, Jiahui Wang, Yaru Zhang, Xirui Li, Wenyu Dong, Yuqing Guo |
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Jazyk: | angličtina |
Rok vydání: | 2021 |
Předmět: |
0301 basic medicine
Antioxidant medicine.medical_treatment Lentinan antioxidant activity T2DM Carbohydrate metabolism Pharmacology medicine.disease_cause chronic ethanol consumption 03 medical and health sciences chemistry.chemical_compound 0302 clinical medicine Diabetes mellitus medicine pancreatic β‐cell failure Insulin Type 2 Diabetes Mellitus Cell Biology Original Articles medicine.disease 030104 developmental biology Nrf‐2 pathway chemistry Apoptosis 030220 oncology & carcinogenesis Molecular Medicine Original Article Oxidative stress |
Zdroj: | Journal of Cellular and Molecular Medicine |
ISSN: | 1582-4934 1582-1838 |
Popis: | Chronic ethanol consumption is a well‐established independent risk factor for type 2 diabetes mellitus (T2DM). Recently, increasing studies have confirmed that excessive heavy ethanol exerts direct harmful effect on pancreatic β‐cell mass and function, which may be a mechanism of pancreatic β‐cell failure in T2DM. 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 ethanol and the possible mechanisms implicated. Functional studies reveal that LNT attenuates chronic ethanol consumption‐induced impaired glucose metabolism in vivo. In addition, LNT ameliorates chronic ethanol consumption‐induced β‐cell dysfunction, which is characterized by reduced insulin synthesis, defected insulin secretion and increased cell apoptosis. Furthermore, mechanistic assays suggest that LNT enhances β‐cell antioxidant capacity and ameliorates ethanol‐induced oxidative stress by activating Nrf‐2 antioxidant pathway. Our results demonstrated that LNT prevents ethanol‐induced pancreatic β‐cell dysfunction and apoptosis, and therefore may be a potential pharmacological agent for preventing pancreatic β‐cell failure associated with T2DM and stress‐induced diabetes. |
Databáze: | OpenAIRE |
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