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Acid Hydrolase - Crossref

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Last Updated: 15 November 2022

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Fatty acid amide hydrolase activity in the dorsal periaqueductal gray attenuates neuropathic pain and associated dysautonomia

The dorsal periaqueductal gray is an integral component of both the pain modulation technique and the acute stress response, and it plays a key role in both analgesia and sympathetic regulation. In neuropathic pain models, inhibition of fatty acid amide hydrolase increases brain concentrations of the endocannabinoid N-arachidonoylethanolamine-based drug and reduces pain-related behavior. Increased FAAH activity in the dPAG has been attributed to increased anxiety and reduced sympathetic tone in neuropathic pain, according to the theory that FAAH inhibition in the dPAG will normalize pain sensation and autonomic function in neuropathic pain. In male and female rats, the effects of systemic or intra-dPAG FAAH inhibition on hyperalgesia and dysautonomia were determined to see this hypothesis. The change in the dPAG's administration of the FAAH inhibitor PF-3845 into the dPAG reduces hyperalgesia activity and sympathetic tone in SNI, which was triggered by SNI.

Source link: https://doi.org/10.1152/ajpregu.00073.2022


Betulinic Acid Hydroxamate is Neuroprotective and Induces Protein Phosphatase 2A-Dependent HIF-1α Stabilization and Post-transcriptional Dephosphorylation of Prolyl Hydrolase 2

We have investigated the mechanism of action of the chemical Betulinic acid hydroxamate, a hypoximimetic derivative of betulinic acid, and its use against striatal neurodegeneration using complementary methods herein. First, we outlined the cellular mechanisms by which BAH modulates the expression of the PHD2 prolyl hydroxylase, thus directly affecting HIF-1-u03b1 stability. BAH's activation by HIF is hampered by okadaic acid and LB-100, implying that a protein phosphatase 2A is involved in BAH's action. BAH stabilized HIF-1u03b1 gene expression in striatal cells carrying a mutated form of the huntingtin protein, which was also shielded against mitochondrial toxin-induced cytotoxicity in mitochondrial cells carrying a mutated form of the huntingtin protein. BAH has a good brain penetrability, and experiments carried out in a mouse model of striatal neurodegeneration induced by 3-nitropropionic acid revealed that BAH has a beneficial brain penetrability, according to the clinical results.

Source link: https://doi.org/10.1007/s13311-021-01089-4


Fatty Acid Amide Hydrolase Deficiency Is Associated with Deleterious Cardiac Effects after Myocardial Ischemia and Reperfusion in Mice

Ischemic cardiomyopathy is a contributor to inflammation and left-ventricular dysfunction. With increased apoptosis and infarctions with worsened LV function in ischemic cardiomyopathy, Cannabinoid type-2 receptor deficiency led to increased apoptosis and infarctions. After ischemia and reperfusion, the aim of our study was to investigate the potential cardioprotective effects of endocannabinoid anandamide. The fatty acid amide hydrolase deficiency mice were occlusion of left anterior descending artery occlusion for three and seven days in a row. a v. The effect of AEA were also triggered by endocannabinoids, as endocannabinoids stimulated PPAR-u03b1 and PPAR-u03b1 were eliminated from AEA's mediated effects by PPAR-u03b1 antagonist GW6471, i. v. Cell sorting was done by chemical analysis, Taqman's RT-qPCR and immune cells were analyzed by fluorescence-activated cell sorting. Compared to WT, FAAHu2212/u2212 mice was significantly elevated in FAAH/u2212 mice, as well as higher macrophage infiltration in infarcted areas, both of which were reversed by GW6471 treatment. Due to PPAR-u03b1 activation, we hypothesize that the rise in endocannabinoids could have partially detrimental effects on cardiomyocyte survival.

Source link: https://doi.org/10.3390/ijms232012690

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* Please keep in mind that all text is summarized by machine, we do not bear any responsibility, and you should always check original source before taking any actions