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Ginsenoside Rb1 improves leptin sensitivity in the prefrontal cortex in obese mice

Journal Article


Abstract


  • Aim: Obesity impairs leptin-induced regulation of brain-derived neurotrophic factor (BDNF) expression and synaptogenesis, which has been considered to be associated with the incidence of neuronal degenerative diseases, cognitive decline, and depression. Ginsenoside Rb1 (Rb1), a major bioactive component of ginseng, is known to have an antiobesity effect and improve cognition. This study examined whether Rb1 can improve central leptin effects on BDNF expression and synaptogenesis in the prefrontal cortex during obesity using an in vivo and an in vitro model. Result: Ginsenoside Rb1 (Rb1) chronic treatment improved central leptin sensitivity, leptin-JAK2-STAT3 signaling, and leptin-induced regulation of BDNF expression in the prefrontal cortex of high-fat diet-induced obese mice. In cultured prefrontal cortical neurons, palmitic acid, the saturated fat, impaired leptin-induced BDNF expression, reduced the immunoreactivity and mRNA expression of synaptic proteins, and impaired leptin-induced neurite outgrowth and synaptogenesis. Importantly, Rb1 significantly prevented these pernicious effects induced by palmitic acid. Conclusion: These results indicate that Rb1 reverses central leptin resistance and improves leptin-BDNF-neurite outgrowth and synaptogenesis in the prefrontal cortical neurons. Thus, Rb1 supplementation may be a beneficial avenue to treat obesity-associated neurodegenerative disorders.

Authors


  •   Wu, Yizhen (external author)
  •   Huang, Xu-Feng
  •   Bell, Christopher (external author)
  •   Yu, Yinghua

Publication Date


  • 2018

Citation


  • Wu, Y., Huang, X., Bell, C. & Yu, Y. (2018). Ginsenoside Rb1 improves leptin sensitivity in the prefrontal cortex in obese mice. CNS Neuroscience and Therapeutics, 24 (2), 98-107.

Scopus Eid


  • 2-s2.0-85033561524

Ro Metadata Url


  • http://ro.uow.edu.au/smhpapers/5181

Number Of Pages


  • 9

Start Page


  • 98

End Page


  • 107

Volume


  • 24

Issue


  • 2

Place Of Publication


  • United Kingdom

Abstract


  • Aim: Obesity impairs leptin-induced regulation of brain-derived neurotrophic factor (BDNF) expression and synaptogenesis, which has been considered to be associated with the incidence of neuronal degenerative diseases, cognitive decline, and depression. Ginsenoside Rb1 (Rb1), a major bioactive component of ginseng, is known to have an antiobesity effect and improve cognition. This study examined whether Rb1 can improve central leptin effects on BDNF expression and synaptogenesis in the prefrontal cortex during obesity using an in vivo and an in vitro model. Result: Ginsenoside Rb1 (Rb1) chronic treatment improved central leptin sensitivity, leptin-JAK2-STAT3 signaling, and leptin-induced regulation of BDNF expression in the prefrontal cortex of high-fat diet-induced obese mice. In cultured prefrontal cortical neurons, palmitic acid, the saturated fat, impaired leptin-induced BDNF expression, reduced the immunoreactivity and mRNA expression of synaptic proteins, and impaired leptin-induced neurite outgrowth and synaptogenesis. Importantly, Rb1 significantly prevented these pernicious effects induced by palmitic acid. Conclusion: These results indicate that Rb1 reverses central leptin resistance and improves leptin-BDNF-neurite outgrowth and synaptogenesis in the prefrontal cortical neurons. Thus, Rb1 supplementation may be a beneficial avenue to treat obesity-associated neurodegenerative disorders.

Authors


  •   Wu, Yizhen (external author)
  •   Huang, Xu-Feng
  •   Bell, Christopher (external author)
  •   Yu, Yinghua

Publication Date


  • 2018

Citation


  • Wu, Y., Huang, X., Bell, C. & Yu, Y. (2018). Ginsenoside Rb1 improves leptin sensitivity in the prefrontal cortex in obese mice. CNS Neuroscience and Therapeutics, 24 (2), 98-107.

Scopus Eid


  • 2-s2.0-85033561524

Ro Metadata Url


  • http://ro.uow.edu.au/smhpapers/5181

Number Of Pages


  • 9

Start Page


  • 98

End Page


  • 107

Volume


  • 24

Issue


  • 2

Place Of Publication


  • United Kingdom