scholarly journals Inhibition of fatty acid amide hydrolase exerts cutaneous anti-inflammatory effects bothin vitroandin vivo

2016 ◽  
Vol 25 (4) ◽  
pp. 328-330 ◽  
Author(s):  
Attila Oláh ◽  
Lídia Ambrus ◽  
Simon Nicolussi ◽  
Jürg Gertsch ◽  
Vilmos Tubak ◽  
...  
Keyword(s):  
Fatty Acid ◽  
Fatty Acid Amide Hydrolase ◽  
Acid Amide ◽  
Anti Inflammatory ◽  
Amide Hydrolase ◽  
Fatty Acid Amide

scholarly journals A Binding Site for Nonsteroidal Anti-inflammatory Drugs in Fatty Acid Amide Hydrolase

2012 ◽  
Vol 135 (1) ◽  
pp. 22-25 ◽  
Author(s):  
Laura Bertolacci ◽  
Elisa Romeo ◽  
Marina Veronesi ◽  
Paola Magotti ◽  
Clara Albani ◽  
...  
Keyword(s):  
Fatty Acid ◽  
Binding Site ◽  
Fatty Acid Amide Hydrolase ◽  
Acid Amide ◽  
Inflammatory Drugs ◽  
Anti Inflammatory ◽  
Amide Hydrolase ◽  
Fatty Acid Amide

scholarly journals Genetic deletion of fatty acid amide hydrolase is associated with anti‐inflammatory cardiovascular phenotype in mice

2008 ◽  
Vol 22 (S1) ◽  
Author(s):  
Sandor Batkai ◽  
Partha Mukhopadhyay ◽  
Mohanraj Rajesh ◽  
Anna Csiszar ◽  
Benjamin F Cravatt ◽  
...  
Keyword(s):  
Fatty Acid ◽  
Fatty Acid Amide Hydrolase ◽  
Acid Amide ◽  
Genetic Deletion ◽  
Anti Inflammatory ◽  
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.

scholarly journals Anti-Inflammatory Effects of Fatty Acid Amide Hydrolase Inhibition in Monocytes/Macrophages from Alzheimer’s Disease Patients

Biomolecules ◽  
2021 ◽  
Vol 11 (4) ◽  
pp. 502
Author(s):  
Valerio Chiurchiù ◽  
Lucia Scipioni ◽  
Beatrice Arosio ◽  
Daniela Mari ◽  
Sergio Oddi ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Fatty Acid ◽  
Cannabinoid Receptors ◽  
Fatty Acid Amide Hydrolase ◽  
Acid Amide ◽  
Anti Inflammatory ◽  
Amide Hydrolase ◽  
Fatty Acid Amide

Growing evidence shows that the immune system is critically involved in Alzheimer’s disease (AD) pathogenesis and progression. The modulation and targeting of peripheral immune mechanisms are thus promising therapeutic or preventive strategies for AD. Given the critical involvement of the endocannabinoid (eCB) system in modulating immune functions, we investigated the potential role of the main elements of such a system, namely type-1 and type-2 cannabinoid receptors (CB1 and CB2), and fatty acid amide hydrolase (FAAH), in distinct immune cell populations of the peripheral blood of AD patients. We found that, compared to healthy controls, CB1 and CB2 expression was significantly lower in the B-lymphocytes of AD patients. Moreover, we found that CB2 was significantly lower and FAAH was significantly higher in monocytes of the same subjects. In contrast, T-lymphocytes and NK cells did not show any variation in any of these proteins. Of note, monocytic CB2 and FAAH levels significantly correlated with clinical scores. Furthermore, the pharmacological inactivation of FAAH in monocytes and monocyte-derived macrophages obtained from AD patients was able to modulate their immune responses, by reducing production of pro-inflammatory cytokines such as TNF-α, IL-6 and IL-12, and enhancing that of the anti-inflammatory cytokine IL-10. Furthermore, FAAH blockade skewed AD monocyte-derived macrophages towards a more anti-inflammatory and pro-resolving phenotype. Collectively, our findings highlight a central role of FAAH in regulating AD monocytes/macrophages that could be of value in developing novel monocyte-centered therapeutic approaches aimed at promoting a neuroprotective environment.

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