R- flurbiprofen attenuates experimental autoimmune encephalomyelitis in mice - Schmitz - 2. EMBO Molecular Medicine. Introduction. R- flurbiprofen, also known as tarenflurbil, is a 2- aryl propionic acid, which has been marketed for the treatment of pain and inflammation together with its S- enantiomer as a racemate. If you use FlowJo (like many flow. Scanner Internet Archive HTML5 Uploader 1.6.1. Oct 5, 2015 10/15. S- flurbiprofen is a potent inhibitor of cyclooxygenases (COX) resulting in non- specific inhibition of prostaglandin synthesis. R- flurbiprofen itself is at least 1. COX- inhibitor (Geisslinger et al, 2. However, R- flurbiprofen reduces pain and inflammation in humans (Lotsch et al, 1. Sprague–Dawley rats (Bishay et al, 2. Geisslinger et al, 1. Data were analyzed using FlowJo software (v. 10) and presented as percentage of peripheral blood mononuclear cells. Guo G, Morrissey J, McCracken R. Tegeder et al, 2. R- to S- flurbiprofen. R- flurbiprofen is almost free of the side- effects typical of classical NSAIDs, such as gastrointestinal or renal toxicity (Holzer et al, 2. Its mechanisms of action involve inhibition of the transcription factors NF- . In particular, R- flurbiprofen treatment after peripheral nerve injury prevents microglia from adopting a phagocyte- like activated phenotype and thereby blocks the neuroinflammatory component of neuropathic pain (Bishay et al, 2. Either as a consequence of the pro- endocannabinoid effects or possibly directly, R- flurbiprofen increases activation of the peroxisome proliferator activated receptors, PPAR. And recently, racemic flurbiprofen was also found to prevent ER stress and leptin resistance and was suggested to provide anti- obesity activity (Hosoi et al, 2. Because of the beneficial anti- inflammatory efficacy and essential lack of toxicity, R- flurbiprofen has been evaluated as a potential remedy in Alzheimer's disease with some success in clinical trials (Wilcock et al, 2. The rationale for these studies was a . Consequently, long- term treatment with R- flurbiprofen of amyloid peptide- overexpressing mice, before appearance of cognitive dysfunction, resulted in a reduction of brain plaque formation, A. Under oxidative stress conditions, it reduced nitrite/nitrate levels and lipid peroxidation in the brain and enhanced the release of the anti- inflammatory interleukin- 1. Lopez- Villodres et al, 2. The beneficial effects of the drug may be partly lost in the aging brain (Bishay et al, 2. Alzheimer's disease because efficacy in clinical phase III trials was insufficient (Green et al, 2. This also holds true for another indication, prostate cancer, for which it was studied based on pre- clinical studies in the TRAMP mouse prostate cancer model, in which R- flurbiprofen was able to reduce the incidence of prostate tumors and metastases (Wechter et al, 2. Hence, R- flurbiprofen has some beneficial, mostly weak, but potentially useful molecular effects, and it is basically free of major toxicity even at high clinical doses and on long- term treatment (Galasko et al, 2. Its immunomodulatory effects, silencing of microglia and the regulatory effects on the endocannabinoid system prompted us to study the effects of R- flurbiprofen in experimental autoimmune encephalomyelitis (EAE) models of multiple sclerosis in mice. The primary hypothesis was that R- flurbiprofen may be useful in the treatment of MS- associated pain, because it reduces neuropathic pain in other models and because cannabis is known to be often the only effective medication for MS- associated pain. The results show that R- flurbiprofen indeed reduced EAE- evoked hyperalgesia in primary progressive PP- EAE in C5. BL6/J mice and in relapsing- remitting RR- EAE in SJL mice. Most strikingly, however, R- flurbiprofen prevented or reduced the severity of EAE in both models in terms of clinical scores, spinal cord inflammation and cell invasion, gene regulation, encephalitis and optic neuritis and was associated with an increase in regulatory and inhibitory T cells and of the inhibitory cytokine IL- 1. Results. Prevention and cure of clinical EAE in C5. BL6/J and SJL mice with R- flurbiprofen. Effects of the early and late onset of treatment with R- flurbiprofen were assessed in C5. BL6/J mice (Fig 1. A–D) that develop a non- remitting form of the disease, and in SJL mice (Fig 1. E–G) that develop a relapsing- remitting (RR)- EAE. R- flurbiprofen completely prevented the development of clinical EAE scores in C5. BL6/J mice when the treatment was started within 3 days after immunization (Fig 1. A and B). This regimen is referred to as preventive treatment. The effect was dose- dependent (Fig 1. B), and the minimum daily dose for complete prevention was 5 mg/kg/day. S- flurbiprofen, at 1. EAE scores (Fig 1. B). Effects of R- flurbiprofen were comparable to those of fingolimod (FTY7. Fig 1. B). R- flurbiprofen also significantly reduced clinical EAE scores in C5. BL6/J mice when treatment was started shortly before onset of clinical manifestations, referred to as semi- therapeutic (1. Fig 1. C) and reduced clinical scores when the treatment was initiated after full development of the disease on day 1. Fig 1. D). For the latter regimen, animals were allocated to R- flurbiprofen or vehicle as score- matched pairs according to their score on day 1. Figure 1. Attenuation of clinical EAE scores by R- flurbiprofen. Time courses of the clinical scores (means . C5. 7BL6/J mice develop a primary progressive EAE (PP- EAE) and SJL/J a relapsing- remitting RR- EAE. 7 Advanced Flow Cytometry Data Analysis Tips For Multi. James McCracken is the Technical Director of the University. 10 FlowJo Version X Hacks That Will. Pregnancy and Preeclampsia Affect Monocyte Subsets in. Pregnancy and Preeclampsia Affect Monocyte Subsets in Humans. Scores: Score 0, no obvious changes in motor functions; score 0. Treatment started 3 days after immunization and was continuously administered in the drinking water (n = 1. ANOVA for . Treatment started 3–4 days before onset of clinical scores, that is, 7–8 after immunization. Treatment started after full development of the disease 1. Animals were allocated as score- matched pairs to the vehicle or R- flurbiprofen group. R- flurbiprofen or vehicle was administered via drug or vehicle soaked sweet cornflakes (n = 1. ANOVA for . The insert in (D) shows the mean body weight of the last 3 treatment days (n = 1. Student's t- test, P = 0. EAE scores on preventive treatment with R- flurbiprofen (5 mg/kg/day) or vehicle. Flowjo CompensationFlowjo Version 10Treatment started 3 days after immunization and was continuously administered in the drinking water (n = 1. ANOVA for . Treatment started on day 1. Animals were allocated to the treatment groups as score- matched pairs based on the severity of the first flare of the disease. Only mice with scores . R- flurbiprofen significantly improved the Rota Rod running performance in these mice during the first remission of the disease, during which all mice had no or minor clinical scores (Fig 1. F). In addition, R- flurbiprofen significantly reduced the EAE relapse rate and severity of RR- EAE scores when the treatment was started very late, 1. Fig 1. G). The mice were allocated to the treatment groups as matched pairs, according to the severity of the first peak. This regimen is referred to as late- therapeutic. The results of statistical comparisons (rm- ANOVA or unpaired two- sided Student's t- tests), the number of animals and P- values are shown in Fig 1 in the respective graphs. Attenuation of nociceptive hypersensitivity in the EAE model. R- flurbiprofen attenuates neuropathic pain in rodents after nerve injury (Bishay et al, 2. MS- associated pain. To test this hypothesis, nociception was analyzed in EAE mice before the onset of clinical scores and during remissions. In C5. 7BL6/J mice, R- flurbiprofen administration (1. This treatment strongly reduced heat (Fig 2. A) and mechanical (Fig 2. B) hyperalgesia, which developed 4–5 days after immunization in vehicle treated mice. R- flurbiprofen also transiently reduced cold allodynia (Fig 2. C). The tail flick assay did not reveal an EAE- evoked hypersensitivity but rather a subtle increase in the reflex time, which was not significantly altered by R- flurbiprofen (Fig 2. D). In SJL mice, treatment with R- flurbiprofen and vehicle was started in score- matched pairs during the first remission of the disease. Under this late- treatment paradigm, R- flurbiprofen significantly reduced nociceptive hypersensitivity during the second remission (Fig 2.
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