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Cordycepin protects islet β-cells against glucotoxicity and lipotoxicity via modulating related proteins of ROS/JNK

Baiyi Yan1, Yanchun Gong1, Wei Meng2

  • 1School of Life Science, Jiangxi Science & Technology Normal University, Nanchang, Jiangxi 330013, PR China.

Biomedicine & Pharmacotherapy = Biomedecine & Pharmacotherapie
|April 26, 2023
PubMed

Insights

Cordycepin, a compound from Cordyceps militaris, protects pancreatic islet cells from high glucose/lipid damage. This natural compound improves insulin secretion and cell survival, offering potential for type 2 diabetes mellitus treatment.

Area of Science:

  • Endocrinology
  • Molecular Biology
  • Pharmacology

Background:

  • Type 2 diabetes mellitus (T2DM) involves pancreatic beta cell dysfunction, reducing insulin synthesis and secretion.
  • Glucotoxicity and lipotoxicity exacerbate beta cell dysfunction in T2DM.

Purpose of the Study:

  • To investigate the protective effects of cordycepin against high glucose/lipid-induced toxicity in INS-1 pancreatic beta cells.
  • To elucidate the underlying molecular mechanisms of cordycepin's action.

Main Methods:

  • INS-1 cells were exposed to high glucose and lipid conditions.
  • Cordycepin treatment was applied to assess its impact on cell viability, energy metabolism, and insulin secretion.
  • Mechanisms involving reactive oxygen species (ROS), ATP levels, calcium (Ca2+) concentration, and apoptosis pathways (JNK, cytochrome c, Caspase-3) were analyzed.

Main Results:

  • Cordycepin enhanced INS-1 cell viability and energy metabolism.
  • It promoted insulin synthesis and secretion.
  • Cordycepin reduced intracellular ROS, increased ATP, stabilized cell membrane potential and Ca2+ levels.
  • It inhibited apoptosis by downregulating the ROS/JNK mitochondrial pathway and upregulating PDX-1.

Conclusions:

  • Cordycepin protects pancreatic islet cells from glucotoxicity and lipotoxicity by inhibiting apoptosis via the ROS/JNK pathway.
  • It improves pancreatic islet cell function, suggesting potential therapeutic applications for T2DM.
Keywords:
ApoptosisCordycepinDiabetesGlucotoxicityINS-1 cellLipotoxicity

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