Passiflora incarnata L. (Passionflower) extracts elicit GABA currents in hippocampal neurons in vitro, and show anxiogenic and anticonvulsant effects in vivo, varying with extraction method.

Potential mechanisms of Passiflora incarnata extracts and the effect of extraction methods on ingredients and biological effects were explored. Using the same batch of plant material, total flavonoid yields as measured by high-performance liquid chromatography coupled to diode array detection (HPLC-DAD) increased substantially with hot versus cold extraction methods. Whole Passiflora extract induced prominent, dose-dependent direct GABA(A) currents in hippocampal slices, but the expected modulation of synaptic GABA(A) currents was not seen. GABA was found to be a prominent ingredient of Passiflora extract, and GABA currents were absent when amino acids were removed from the extract. Five different extracts, prepared from a single batch of Passiflora incarnata, were administered to CF-1 mice for 1 week in their drinking water prior to evaluation of their behavioral effects. Anticonvulsant effects against PTZ-induced seizures were seen in mice that received 2 of the 5 Passiflora extracts. Instead of the anxiolytic effects described by others, anxiogenic effects in the elevated plus maze were seen in mice receiving any of the 5 Passiflora extracts.

In vivo evaluation of piperine and synthetic analogues as potential treatments for vitiligo using a sparsely pigmented mouse model.

BACKGROUND: Piperine and its analogues have been reported to stimulate melanocyte replication in vitro and may be useful in treating the depigmenting disease, vitiligo. OBJECTIVE: To investigate the ability of piperine (PIP) and three analogues to stimulate pigmentation in a strain of sparsely pigmented mice. METHODS: The test compounds were PIP [5-(3,4-methylenedioxyphenyl)-2,4-pentadienoylpiperidine], tetrahydropiperine [THP, 5-(3,4-methylenedioxyphenyl)-pentanoylpiperidine], a cyclohexyl analogue of piperine [CHP, 5-(3,4-methylenedioxyphenyl)-2,4-pentadienoylcyclohexylamine], and reduced CHP [rCHP, 5-(3,4-methylenedioxyphenyl)-2,4-pentanoylcyclohexylamine]. Sparsely pigmented, HRA/Skh-II mice were randomized to receive topical treatment with test compounds or vehicle twice a day for five days a week, with or without ultraviolet (UV) irradiation on 3 days a week. Treatment was either continuous or interrupted to evaluate fading and repigmentation. Skin inflammation and pigmentation were evaluated regularly during treatment. DOPA+ melanocytes were determined histologically at the termination of treatment. RESULTS: Four weeks of treatment with one of the compounds PIP, THP or rCHP, but not CHP, induced greater pigmentation than vehicle with low levels of inflammation. Additional exposure to UVR led to darker pigmentation than did the compound or UVR alone, and greater numbers of DOPA+ melanocytes were found. The combination produced an even pigmentation pattern, contrasting with the speckled, perifollicular pattern produced by UVR alone. Treatment interruption led to a decrease in pigmentation but not its loss. Repigmentation was achieved by administering one of the compounds, UVR or both, and occurred faster than in naïve mice. CONCLUSIONS: Treatment with PIP, THP or rCHP and UVR induced a marked pigmentation response in HRA/Skh-II mice, with clinically better results than UVR alone. This result supports the potential use of these compounds in treating vitiligo.