Kurkuma a fluoksetyna to już na koniec, prawie koniec

Dostałem od Ryszarda “małe” podsumowanie dotyczące porównania kurkumy i fluoksetyny. Oto one:

1.W badaniach tych potraktowano kurkumę jako antydepresanta i jako czynnik wywołujący neurogenezę

2.Porównano terapię fluoksetynę i kurkumą

3.Wyniki jakie otrzymano to:

- kurkuma z pewnością jest aktywnym antydepresantem

-kurkuma uzyskuje wyniki podobne do tych jakie uzyskuje się w testach fluoksetyną

-kurkuma wpływa na plastyczność mózgu a dzięki temu na efekt neurogenezy poprzez regulację serotoniny 5HT, podobnie jak ma to miejsce w przypadku fluoksetyny

 

Acta Pol Pharm. 2011 Sep-Oct;68(5):769-75.

Evaluation of antidepressant like activity of curcumin and its combination with fluoxetine and imipramine: an acute and chronic study.

Sanmukhani J, Anovadiya A, Tripathi CB.

Source

Department of Pharmacology, Government Medical College, Bhavnagar – 364001, Gujarat, India.

Abstract

Curcumin is the active ingredient of commonly used spice Curuma longa Linn. In the present study, the antidepressant like activity of curcumin and its combination with fluoxetine and imipramine was studied in acute model (three doses 24, 5 and 1 h before test) of forced swimming test (FST) in glass jar and tail suspension test (TST) in mice and in chronic model (14 day study) of FST with water wheel in rats. All the tests were carried out in the following seven groups (n = 6 in each group), drugs being given orally (doses for mice): Group 1 (vehicle), group 2 (curcumin 50 mg/kg), group 3 (curcumin 100 mg/kg), group 4 (fluoxetine 20 mg/kg), group 5 (imipramine 15 mg/kg), group 6 (curcumin 100 mg/kg plus fluoxetine 20 mg/kg) and group 7 (curcumin 100 mg/kg plus imipramine 15 mg/kg). Equivalent doses for rats were used. Both the acute model of FST and TST, and the chronic model of FST with water wheel showed significant antidepressant like activity of curcumin in 100 mg/kg dose as compared to vehicle control (p < 0.05). The effect of curcumin (100 mg/kg) was similar to that of fluoxetine and imipramine (p > 0.05) but its addition to fluoxetine and imipramine did not improve their antidepressant activity (p > 0.05). Curcumin increased both the swimming and climbing behavior in FST, thus its antidepressant like activity could be due to an increase in serotonin, norepinephrine and dopamine levels in the brain. Curcumin can be a useful antidepressant especially in cases which respond to drugs having mixed effects on serotonin and catecholamines levels in the brain.

PMID:

21928724

[PubMed – indexed for MEDLINE]

 

and this:

 

J Neurochem. 2011 Sep;118(5):784-95. doi: 10.1111/j.1471-4159.2011.07356.x. Epub 2011 Jul 18.

Curcumin prevents corticosterone-induced neurotoxicity and abnormalities of neuroplasticity via 5-HT receptor pathway.

Xu Y,Li S,Vernon MM,Pan J,Chen L,Barish PA,Zhang Y,Acharya AP, Yu J, Govindarajan SS, Boykin E, Pan X, O’Donnell JM, Ogle WO.

Source

J. Crayton Pruitt Family Department of Biomedical Engineering, University of Florida, Gainesville, Florida 32611, USA. yingxufl@yahoo.com

Abstract

Curcumin, a major active component of Curcuma longa, possesses antioxidant and neuroprotective activities. The present study explores the mechanisms underlying the neuroprotective effect of curcumin against corticosterone and its relation to 5-hydroxy tryptamine (5-HT) receptors. Exposure of cortical neurons to corticosterone results in decreased mRNA levels for three 5-HT receptor subtypes, 5-HT(1A), 5-HT(2A) and 5-HT(4), but 5-HT(1B,) 5-HT(2B), 5-HT(2C), 5-HT(6) and 5-HT(7) receptors remain unchanged. Pre-treatment with curcumin reversed this effect on mRNA for the 5-HT(1A) and 5-HT(4) receptors, but not for the 5-HT(2A) receptor. Moreover, curcumin exerted a neuroprotective effect against corticosterone-induced neuronal death. This observed effect of curcumin was partially blocked by either 5-HT(1A) receptor antagonist p-MPPI or 5-HT(4) receptor antagonist RS 39604 alone; whereas, the simultaneous application of both antagonists completely reversed the effect. Curcumin was also found to regulate corticosterone-induced morphological changes such as increases in soma size, dendritic branching and dendritic spine density, as well as elevate synaptophysin expression in cortical neurons. p-MPPI and RS 39604 reversed the effect of curcumin-induced change in neuronal morphology and synaptophysin expression of corticosterone-treated neurons. In addition, an increase in cyclic adenosine monophosphate (cAMP) level was observed after curcumin treatment, which was further prevented by RS 39604, but not by p-MPPI. However, curcumin-induced elevation in protein kinase A activity and phosphorylation of cAMP response element-binding protein levels were inhibited by both p-MPPI and RS 39604. These findings suggest that the neuroprotection and modulation of neuroplasticity exhibited by curcumin might be mediated, at least in part, via the 5-HT receptor-cAMP-PKA-CREB signal pathway.

© 2011 The Authors. Journal of Neurochemistry © 2011 International Society for Neurochemistry