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Salidroside Alleviates Diabetic Cognitive Dysfunction Via B3galt2/F3/Contactin Signaling Pathway in Mice.

Pan Lv1, Zhongfu Zuo2, Wenqiang Liu1

  • 1Department of Anatomy, Histology and Embryology, Jinzhou Medical University, Jinzhou, China.

Neuroscience
|December 12, 2022
PubMed
Summary

This study reveals that reduced β-1, 3-galactosyltransferase 2 (B3galt2) exacerbates diabetic cognitive dysfunction (DCD). Restoring B3galt2 levels protects against neuronal damage and cognitive decline in diabetic mice.

Keywords:
F3/Contactinapoptosiscognitive dysfunctiondiabetessalidrosideβ-1, 3-galactosyltransferase 2

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Area of Science:

  • Neuroscience
  • Glycobiology
  • Endocrinology

Background:

  • Diabetes mellitus is associated with cognitive impairment, affecting neuronal function.
  • β-1, 3-galactosyltransferase 2 (B3galt2) plays a role in glycosylation and neuronal processes.
  • The specific involvement of B3galt2 in diabetic cognitive dysfunction (DCD) remains unexplored.

Purpose of the Study:

  • To investigate the role of B3galt2 in the pathogenesis of DCD.
  • To explore the potential therapeutic effects of salidroside (SAL) on DCD.
  • To elucidate the molecular mechanisms underlying B3galt2's function in DCD.

Main Methods:

  • Utilized a diabetic mouse model (C57BL/6J) to assess cognitive function and B3galt2 expression.
  • Manipulated B3galt2 levels through overexpression and genetic deficiency (B3galt2+/- mice).
  • Employed immunohistochemistry to examine B3galt2 and F3/Contactin co-localization in the hippocampus and assessed neuronal damage, synapsin protection, and apoptosis.

Main Results:

  • Diabetic mice exhibited cognitive deficits and decreased B3galt2 expression.
  • Overexpression of B3galt2 ameliorated cognitive decline and hippocampal neuronal damage in diabetic mice.
  • B3galt2 regulated F3/Contactin expression, protected synapsin, and reduced neuronal apoptosis.
  • Salidroside (SAL) treatment alleviated DCD and normalized B3galt2 expression in diabetic mice.

Conclusions:

  • The inhibition of the B3galt2/F3/Contactin pathway contributes to diabetic cognitive dysfunction.
  • B3galt2 plays a protective role against neuronal damage and cognitive decline in diabetes.
  • Salidroside demonstrates therapeutic potential for DCD by modulating the B3galt2/F3/Contactin pathway.