scholarly journals Fatty acid amide hydrolase (FAAH) inhibition enhances memory acquisition through activation of PPAR-  nuclear receptors

2009 ◽  
Vol 16 (5) ◽  
pp. 332-337 ◽  
Author(s):  
C. Mazzola ◽  
J. Medalie ◽  
M. Scherma ◽  
L. V. Panlilio ◽  
M. Solinas ◽  
...  
Keyword(s):  
Fatty Acid ◽  
Nuclear Receptors ◽  
Fatty Acid Amide Hydrolase ◽  
Acid Amide ◽  
Memory Acquisition ◽  
Faah Inhibition ◽  
Amide Hydrolase ◽  
Fatty Acid Amide

scholarly journals The endogenous cannabinoid anandamide has effects on motivation and anxiety that are revealed by fatty acid amide hydrolase (FAAH) inhibition

2008 ◽  
Vol 54 (1) ◽  
pp. 129-140 ◽  
Author(s):  
Maria Scherma ◽  
Julie Medalie ◽  
Walter Fratta ◽  
Subramanian K. Vadivel ◽  
Alexandros Makriyannis ◽  
...  
Keyword(s):  
Fatty Acid ◽  
Fatty Acid Amide Hydrolase ◽  
Acid Amide ◽  
Faah Inhibition ◽  
Amide Hydrolase ◽  
Endogenous Cannabinoid ◽  
Fatty Acid Amide

P4-223: Fatty acid amide hydrolase inhibition enhances learning and memory through activation of PPAR-alpha nuclear receptors

2008 ◽  
Vol 4 ◽  
pp. T736-T737
Author(s):  
Sevil Yasar ◽  
Carmen Mazzola ◽  
Julie Medalie ◽  
Maria Scherma ◽  
Leigh Panlilio ◽  
...  
Keyword(s):  
Fatty Acid ◽  
Learning And Memory ◽  
Nuclear Receptors ◽  
Fatty Acid Amide Hydrolase ◽  
Acid Amide ◽  
Ppar Alpha ◽  
Amide Hydrolase ◽  
Fatty Acid Amide

scholarly journals Anti-Inflammatory Effects by Pharmacological Inhibition or Knockdown of Fatty Acid Amide Hydrolase in BV2 Microglial Cells

Cells ◽  
2019 ◽  
Vol 8 (5) ◽  
pp. 491 ◽  
Author(s):  
Mikiei Tanaka ◽  
Kazuya Yagyu ◽  
Scott Sackett ◽  
Yumin Zhang
Keyword(s):  
Fatty Acid ◽  
Inflammatory Cytokines ◽  
Fatty Acid Amide Hydrolase ◽  
Acid Amide ◽  
Pge2 Production ◽  
Faah Inhibition ◽  
Anti Inflammatory ◽  
Amide Hydrolase ◽  
Bv2 Microglial Cells ◽  
Fatty Acid Amide

Fatty acid amide hydrolase (FAAH) has been recognized as a therapeutic target for several neurological diseases because its inhibition can exert neuroprotective and anti-inflammatory effects by boosting the endogenous levels of N-acylethanolamines. However, previous studies have shown inconsistent results by pharmacological inhibition and genetic deletion of FAAH in response to inflammation. In this study we used two inhibitors, PF3845 and URB597, together with siRNA knockdown to characterize further the effects of FAAH inhibition in BV2 microglial cells. Treatment with PF3845 suppressed lipopolysaccharide (LPS)-induced prostaglandin E2 (PGE2) production, and down-regulated cyclooxygenase-2 and microsomal PGE synthase. PF3845 reduced the expression of pro-inflammatory cytokines but had no effect on the expression of anti-inflammatory cytokines. The anti-inflammatory effects of URB597 were not as potent as those of PF3845. Knockdown of FAAH also suppressed PGE2 production and pro-inflammatory gene expression. Interestingly, FAAH knockdown enhanced expression of anti-inflammatory molecules in both the absence and presence of LPS treatment. The anti-inflammatory effects of FAAH inhibition and knockdown were not affected by the cannabinoid receptor antagonists or the peroxisome proliferator-activated receptor (PPAR) antagonists. Although inhibition and knockdown of FAAH have potent anti-inflammatory effects and possibly lead to the dynamic change of microglial gene regulation, the underlying mechanisms remain to be elucidated.

Sign in / Sign up

Export Citation Format

Share Document