Research and Clinical Trials on Fluoxetine (Prozac, Sarafem)

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This list of current clinical research trials on Fluoxetine (Prozac, Sarafem) is followed by a short set of abstracts from the most recent research articles published on the drug.

Fluoxetine (Prozac, Sarafem) Clinical Research Trials

From our searchable database at ClinicalTrialsFeeds.org, this list includes all the latest information about clinical trials involving Fluoxetine (Prozac, Sarafem).

 

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Current Research Literature on Fluoxetine (Prozac, Sarafem)

Here are abstracts for some of the latest research articles to have appeared on Fluoxetine (Prozac, Sarafem):

Selective serotonin re-uptake inhibitors decrease the cytokine-induced endothelial adhesion molecule expression, the endothelial adhesiveness to monocytes and the circulating levels of vascular adhesion molecules.

Int J Cardiol. 2008 Nov 10;
Lekakis J, Ikonomidis I, Papoutsi Z, Moutsatsou P, Nikolaou M, Parissis J, Kremastinos DT
BACKGROUND: Selective serotonin reuptake inhibitors (SSRIs) exert cardioprotective effects. We examined whether SSRIs a) modulate endothelial cell expression of vascular cell adhesion molecule (VCAM-1), intracellular adhesion molecule (ICAM-1) and adhesiveness to U937 monocytes, b) reduce the circulating levels of these adhesion molecules in vivo. METHODS: We assessed the effect of SSRIs, (citalopram, fluvoxamine and fluoxetine), on TNF-alpha-induced expression of VCAM-1 and ICAM-1 in human aorta endothelial cells and adhesiveness to U937 monocytes. Cells were incubated with TNF-alpha in the absence and in the presence of SSRIs concentrations from 10(-7) M to10(-4) M and the VCAM-1 and ICAM-1 expression was quantified by cell-ELISA. The TNF-alpha-stimulated adhesiveness to U937 monocytes was also assessed. Twenty five patients with chronic heart failure and depression were randomized to receive sertaline 50 mg, p.o., o.d. (n=13) or placebo. At baseline and 3-months after treatment, we measured VCAM-1and ICAM-1 plasma levels. RESULTS: SSRIs decreased the TNF-alpha-induced endothelial expression of VCAM-1 at concentration range 10(-7) M to 10(-4) M (p

The effect of high glucose on SERT, the human plasmalemmal serotonin transporter.

Nutr Neurosci. 2008 Dec; 11(6): 244-50
Gonçalves P, Araújo JR, Martel F
The aim of this work was to investigate the effect of short- and long-term high-glucose exposure on the plasmalemmal serotonin transporter (SERT)-mediated uptake of [(3)H]-serotonin (5-HT) by Caco-2 cells. Short-term exposure of Caco-2 cells to high apical glucose levels (30 mM for 2 h or 40 mM for 1 h) decreased the uptake of [(3)H]-5-HT by 20-30%. On the other hand, long-term (21-24 weeks) exposure of the cells to high (25 mM) glucose caused a 30% increase in the uptake of [(3)H]5-HT. Under these conditions, the affinity of the transporter for 5-HT and noradrenaline was not significantly changed, and the inhibitory potencies of fluoxetine and desipramine were also unchanged. In conclusion, high-glucose levels modulate SERT activity. A short-term exposure of the cells to a high concentration of glucose decreases the activity of the transporter, whereas a longer exposure of the cells to a high concentration of glucose increases the activity of SERT, without interfering with its affinity.

Depressant-like effects of parthenolide in a rodent behavioural antidepressant test battery.

J Pharm Pharmacol. 2008 Dec; 60(12): 1643-50
Pandey DK, Rajkumar R, Mahesh R, Radha R
The anti-serotonergic effects of parthenolide (PTL) demonstrated in platelets inspired the present psychopharmacological investigation, which employs a battery of rodent behavioural assays of depression. In mice, PTL (0.5-2 mg kg(-1)) exhibited dose-dependent depressant-like effects in a forced swim test and a tail suspension test, without affecting the baseline locomotor status. The doses (1 and 2 mg kg(-1)) that induced depressant-like effects were found to significantly reduce 5-hydroxytryptophan-induced head twitch response. Interaction studies revealed that the depressant-like effects of PTL (1 mg kg(-1)) were reversed more efficiently by serotonergic antidepressants (venlafaxine, escitalopram, citalopram, fluoxetine) than by others (desipramine, bupropion) tested. Chronic treatment of PTL (1 and 2 mg kg(-1)) augmented the hyper-emotionality of olfactory bulbectomized rats, when compared with sham rats, as observed in modified open field, elevated plus maze and social interaction paradigms. This study depicts the severe depressogenic potential of PTL (in its pure form) plausibly mediated by platelet/neuronal hypo-serotonergic effects.

Estimation of embryotoxic effect of fluoxetine using embryonic stem cell differentiation system.

Life Sci. 2008 Oct 28;
Kusakawa S, Yamauchi J, Miyamoto Y, Sanbe A, Tanoue A
AIMS: Fluoxetine is an antidepressant drug of the selective serotonin reuptake inhibitor (SSRI) class, which is commonly prescribed to treat a wide spectrum of mood disorders including depression during pregnancy and lactation. Recent studies have proposed a possible association between an increase in major malformations and the maternal use of SSRI drugs during pregnancy. Here, we assess the effects of fluoxetine using a mouse ES cell differentiation system to clarify the possible association. MAIN METHODS: Using a mouse embryonic stem (ES) cell differentiation system, we evaluated cell viability and differentiation affected by fluoxetine. KEY FINDINGS: Fluoxetine adversely affected cell viability and differentiation from undifferentiated ES cells to cardiomyocytes in a dose-dependent manner. The IC(50) values of fluoxetine for ES cells and NIH-3T3 fibroblasts were 1.79 muM and 4.67 muM, respectively, and the ID(50) value for ES cells was 3.79 muM. These results indicate that fluoxetine has strong toxicity evaluated by a mouse embryonic stem cell test (EST). Analysis of tissue-specific markers revealed that fluoxetine potently inhibits mesodermal development, although it promotes ectodermal differentiation in a lineage-specific manner. SIGNIFICANCE: These results using the in vitro ES cell assay system suggest a possible relationship between the teratogenicity of fluoxetine and its molecular mechanism.

Serotonin (5-HT) transporter ligands affect plasma 5-HT in rats.

Ann N Y Acad Sci. 2008 Oct; 1139: 268-84
Rothman RB, Zolkowska D, Baumann MH
Dual dopamine (DA)/serotonin (5-HT)-releasing agents are promising candidate medications for stimulant addiction and other disorders. However, certain 5-HT transporter (SERT) substrates are associated with development of idiopathic pulmonary arterial hypertension (IPAH) and valvular heart disease (VHD). According to the "5-HT hypothesis," SERT substrates increase the risk for developing IPAH and VHD by increasing plasma 5-HT. To test this hypothesis directly, we determined the effects of acute and chronic fenfluramine, and other SERT ligands, on plasma 5-HT in male rats. For acute treatments, rats received i.v. vehicle or test drug (0.3 and 1.0 mg/kg), and serial blood samples were withdrawn. For chronic treatments, vehicle or test drug was infused via osmotic minipump (3 and 10 mg/kg/d) for 2 weeks. On the last day of infusion, rats received i.v. fenfluramine challenge (1 mg/kg), and serial blood samples were withdrawn. Plasma 5-HT was measured using ex vivo microdialysis in whole-blood samples. Baseline plasma 5-HT was

 

This page was last reviewed by Dr Greg Mulhauser, Friday, 4 July 2008.

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