Has anyone heard about this herbal agent ?
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4358691/
"With regard to improvements in sexual dysfunction, it is possible that agents of R. damascena oil have an antagonistic effect on the stimulation of the postsynaptic 5-HT2 and 5-HT3 receptors30–32 and that these agents have an antago nistic effect on the corticolimbic 5-HT receptors, which are responsible for increasing sexual desire, ejaculation, and orgasm.34,35 Additionally, it is possible that the agents of R. damascena agonistically increase the release of dopamine and norepinephrine in the substantia nigra,31,32 as well as disinhibiting nitric oxide synthase.33 Further, R. damascena oil seems to have an antimicrobial effect, and has been reported to protect neurons against amyloid β toxicity, a major pathological component of Alzheimer’s disease, and to protect rats against seizures. More specifically, it is suggested that the agent glycoside quercetin is also responsible for improving neuronal activity, probably by inducing the expression of synaptic proteins synaptotagmin and post-synaptic density protein-95, at least in cultured rat cortical neurons.65 Likewise, quercetin has been shown to reduce behavioral deficiencies, restore astrocytes and microglia, and reduce serotonin metabolism in a 3-nitropropionic acid-induced rat model of Huntington’s Disease.66 Last, Merzoug et al67 reported that quercetin mitigated Adriamycin-induced anxiety- and depression-like behaviors, immune dysfunction, and brain oxidative stress in rats.
With regard to the glycoside kaempferol, evidence from animal studies has shown an antidepressant and modulating effect on brain-derived neurotrophic factor and β amyloid in the neurons and hippocampus of double TgAD mice.68
Overall, research on animal models suggest that both quercetin and kaempferol, two of the main agents of R. damascena oil, seem to have beneficial influences on symptoms of depression at the molecular level.
Moreover, we also observe that explaining the occurrence and maintenance of MDD in terms of monoamine deficiency is just one of several putative pathways by which MDD might be explained neurophysiologically and neuroendocrinologically. In this regard, more recently efforts have been made to further investigate the roles of the neuropeptide brain-derived neurotrophic factor on MDD,10,69,70 on ketamine,71 and statins.72–75 With regard to statins, by using a mouse model, Ludka et al16 observed that after acute atorvastatin treatment, the antidepressant effect seemed to be explained via the L-argininenitric oxide-cyclic guanosine mono-phosphate pathway; atorvastatin seemed to inhibit NMDA (N-methyl-d-aspartatic acid) receptors and NO-cGMP (nitric oxide-cyclic guanosine monophosphate) synthesis, leading to a down-regulation of excitatory processes. On a behavioral level, this down-regulation seems to be reflected in a reduction of symptoms of depression. However, it remains unclear to what extent the new pathways explaining MDD neurophysiologically and neuroendocrinologically may help to better understand the influence of the agents of R. damascena oil on both symptoms of depression and sexual dysfunction."





