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Naringin Protects Pancreatic β‐Cells Against Oxidative Stress‐Induced Apoptosis by Inhibiting Both Intrinsic and Extrinsic Pathways in Insulin‐Deficient Diabetic Mice
Author(s) -
Lim Ye Jin,
Kim Jung Ho,
Pan Jeong Hoon,
Kim Jae Kyeom,
Park TaeSik,
Kim Young Jun,
Lee Jin Hyup,
Kim Jun Ho
Publication year - 2018
Publication title -
molecular nutrition and food research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.495
H-Index - 131
eISSN - 1613-4133
pISSN - 1613-4125
DOI - 10.1002/mnfr.201700810
Subject(s) - naringin , oxidative stress , reactive oxygen species , streptozotocin , apoptosis , insulin , pharmacology , insulin receptor , diabetes mellitus , signal transduction , endocrinology , medicine , chemistry , insulin resistance , biology , microbiology and biotechnology , biochemistry , chromatography
Scope Oxidative stress has been suggested to play a central role in the pathogenesis of diabetes, as well as other metabolic disorders. Naringin, a major flavanone glycoside in citrus species, has been shown to display strong antioxidant potential in in vitro and in vivo models of oxidative stress; however, the underlying protective mechanisms in diabetes are unclear. Methods and results To study the protective effects and molecular mechanisms of naringin in preventing islet dysfunction and diabetes, we examined glucose homeostasis, β‐cell apoptosis, and inflammatory response in insulin‐deficient diabetic mice exposed to acute oxidative stress with streptozotocin (STZ). Naringin dose‐dependently ameliorated hyperglycemia and islet dysfunction in insulin‐deficient diabetic mice. Naringin counteracted STZ‐induced β‐cell apoptosis by inhibiting both the intrinsic (mitochondria‐mediated) and extrinsic (death receptor‐mediated) pathways. Furthermore, these protective effects were associated with suppression of DNA damage response and nuclear factor–kappa B– and mitogen–activated protein kinase–mediated signaling pathways, as well as reduction of reactive oxygen species accumulation and pro‐inflammatory cytokine production in the pancreas. Conclusion Taken together, our study provides insights into the underlying mechanisms through which naringin protects the pancreatic β‐cells against oxidative stress‐induced apoptosis.