Green tea protects against hippocampal neuronal apoptosis in diabetic encephalopathy by inhibiting JNK/MLCK signaling

Mol Med Rep. 2021 Aug;24(2):575. doi: 10.3892/mmr.2021.12214. Epub 2021 Jun 16.

Abstract

Although diabetic encephalopathy (DE) is a major late complication of diabetes, the pathophysiology of postural instability in DE remains poorly understood. Prior studies have suggested that neuronal apoptosis is closely associated with cognitive function, but the mechanism remains to be elucidated. Green tea, which is a non‑fermented tea, contains a number of tea polyphenols, alkaloids, amino acids, polysaccharides and other components. Some studies have found that drinking green tea can reduce the incidence of neurodegenerative diseases and improve cognitive dysfunction. We previously found that myosin light chain kinase (MLCK) regulates apoptosis in high glucose‑induced hippocampal neurons. In neurodegenerative diseases, including Alzheimer's disease and Parkinson's disease, activation of the JNK signaling pathway promotes neuronal apoptosis. However, the relationship between JNK and MLCK remains to be elucidated. Green tea serum was obtained using seropharmacological methods and applied to hippocampal neurons. In addition, a type 1 diabetes rat model was established and green tea extract was administered, and the Morris water maze test, Cell Counting Kit‑8 assays, flow cytometry, western blotting and terminal deoxynucleotidyl transferase‑mediated dUTP nick end‑labelling assays were used to examine the effects of green tea on hippocampal neuronal apoptosis in diabetic rats. The results demonstrated that green tea can protect against hippocampal neuronal apoptosis by inhibiting the JNK/MLCK pathway and ultimately improves cognitive function in diabetic rats. The present study provided novel insights into the neuroprotective effects of green tea.

Keywords: JNK/myosin light chain kinase signaling pathway; cognitive function; diabetic encephalopathy; green tea; hippocampal neuron apoptosis.

MeSH terms

  • Animals
  • Apoptosis / drug effects*
  • Brain Diseases / drug therapy
  • Brain Diseases / metabolism*
  • Cells, Cultured
  • Cognitive Dysfunction / drug therapy
  • Diabetes Mellitus, Experimental / complications
  • Diabetes Mellitus, Experimental / metabolism*
  • Hippocampus / cytology
  • Hippocampus / drug effects*
  • Hippocampus / metabolism
  • In Situ Nick-End Labeling
  • JNK Mitogen-Activated Protein Kinases / metabolism
  • MAP Kinase Signaling System / drug effects*
  • Male
  • Maze Learning / drug effects
  • Models, Animal
  • Myosin-Light-Chain Kinase / metabolism
  • Neurons / drug effects*
  • Neurons / metabolism
  • Neuroprotective Agents / pharmacology
  • Plant Extracts / pharmacology*
  • Rats
  • Rats, Sprague-Dawley
  • Tea / chemistry

Substances

  • Neuroprotective Agents
  • Plant Extracts
  • Tea
  • Myosin-Light-Chain Kinase
  • JNK Mitogen-Activated Protein Kinases

Grants and funding

The present study was supported by the National Natural Science Foundation of China (grant nos. 81960151 and 81960822), the Guizhou Provincial Department of Education Innovation Group Major Research Project [grant no. (2018)021] and the Guizhou Provincial Science and Technology Department Support Program [grant no. (2019)2802].