Language:
  
[Sign in] [Register]   

EIAab logo

EIAab news detail, please contact eiaab@eiaab.com if you have any questions about online orders and payment.
Beta-caryophyllene alleviates diet-induced neurobehavioral changes in rats: The role of CB2 and PPAR-γ receptors
Update time:2018-11-29 18:58:13   【 Font: Large  Medium Small

Abstract

Background and purpose: Insulin resistance (IR) and obesity predispose diseases such as diabetes, cardiovascular and neurodegenerative disorders. Beta-caryophyllene (BCP), a natural sesquiterpene, exerts neuroprotective, anxiolytic and antidepressant effects via its selective agonism to cannabinoid receptor 2 (CB2R). BCP was shown to have an anti-diabetic effect, however, the implication of CB2R is yet to be elucidated. A link between CB2R agonism and PPAR-γ activation has been discussed, but the exact mechanism is not well-defined. This study was designed to examine the role of BCP in improving diet-induced metabolic (insulin resistance), neurobehavioral (anxiety, depression and memory deficit), and neurochemical (oxidative, inflammatory and neurotrophic factor) alterations in the prefrontal cortex of obese rats’ brain. The involvement of CB2R and/or PPAR-γ dependent activity was also investigated.

Experimental approach: Male Wistar rats were fed a high fat/fructose diet (HFFD) for 12 weeks to induce IR and obesity. Rats were treated with BCP for the last 4 weeks. Either CB2R antagonist AM630 or PPAR-γ antagonist BADGE was administered before BCP treatment to study the mechanism of BCP actions.

Key results: Beta-caryophyllene alleviated HFFD-induced IR, oxidative-stress, neuroinflammation and behavioral changes. The anxiolytic, anti-oxidant and anti-inflammatory effects of BCP were mediated by both PPAR-γ and CB2R. The effects of BCP on glycemic parameters seem to be CB2R-dependent with the non-significant role of PPAR-γ. Furthermore, BCP-evoked antidepressant and memory improvement are likely mediated only via CB2R, mainly by upregulation of PGC-1α and BDNF.

Conclusion: This study suggests the potential effect of BCP in treating HFFD-induced metabolic and neurobehavioral alterations. BCP seems to activate PPAR-γ in a ligand-independent manner, via upregulation and activation of PGC-1α. The BCP activation of PPAR--γ seems to be CB2R-dependent.

Cited products
Source:Biomedicine & Pharmacotherapy      by D A. Youssef, H M. El-Fayoumi, M F. Mahmoud.
Hot Genes
ALCAM ACE KSR2 ASPRO C19orf80 Gdf5 Trap1a Atf2
Top Searches
Ubiquitin ELISA Ubiquitin-protein ligase metalloproteinase Asprosin Tumor necrosis TRAP1A vitamin d
Why choose EIAAB
Our products have been quoted by many publications in famous journals such as Cell; Cell Metabolism; Hepatology; Biomaterials.more
Further Information
About us Protein center Bank account Distributors Terms & Conditions Career eiaab.cn

Copyright & copy www.eiaab.com2006-2016 All Rights Reserved    EIAab         Email:eiaab@eiaab.com

Twitter