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Halophyte plants are salt-tolerant and are acclimated for growth in saline soils such as along coastal areas. Among the halophytes, the Salicornia species have been used as both folk medicine and functional food for many years due to their high levels of bioactive compounds with supposed anti-inflammatory and antioxidative effects. However, the properties of Salicornia bioactive extracts on pain and itching still remain unclear. In this study, 30 healthy volunteers were randomized to treatments with 10% Salicornia-based cream or placebo cream for 24 or 48 h. On day 0, and 24 or 48 h post cream application, cold/heat detection and pain thresholds, mechanical pain thresholds and sensitivity, trans-epidermal water loss, histamine- and cowhage-evoked itch, and micro-vascular reactivity (neurogenic inflammation) were assessed to evaluate the analgesic, anti-pruritogenic and vasomotor effects. Skin permeability was reduced in the Salicornia-treated area for 48 h compared with 24 h application ( p -value < 0.05). After 48 h of application, a decrease in mechanical-evoked itching (hyperkinesis) compared with 24 h treatment ( p -value < 0.05) and increased warm detection and heat pain thresholds ( p -value < 0.05) was found. Histamine-induced neurogenic inflammation showed a significant reduction in the cream-treated areas after 48 h compared with 24 h ( p -value < 0.05). The results of this study indicate the overall inhibitory effect of Salicornia on hyperkinesis (mechanically evoked itch), the analgesic effect on thermal sensation, and modulation of the skin barrier architecture. Further studies are needed for the assessment of the long-term effects.

Experimental models of prolonged pain hypersensitivity in humans are desirable for screening novel analgesic compounds. In this study, heat stimuli were applied in ultraviolet-B (UVB)-irradiated skin and in the UVB-irradiated skin combined with nerve growth factor (NGF)-injected muscle to investigate 1) whether the evoked mechanical hypersensitivity by UVB irradiation would be prolonged or enhanced following heat rekindling, and 2) whether the combination between cutaneous and muscle hypersensitivity may influence the rekindling effects. Skin sensitization was induced in 25 volunteers by UVB irradiation in areas above the upper-trapezius muscle, low-back or forearm. Muscle sensitization was induced in the low back by bilateral injections of NGF. The area of cutaneous hyperalgesia was evaluated 3 days after the irradiation by mechanical pin-prick stimulation whereas the areas of allodynia were evaluated 1, 2 and 3 days after irradiation by von Frey hair assessments. Cutaneous heat stimulation (40°C for 5 min) was performed on the 3(rd) day to investigate its effect on the areas of cutaneous allodynia and hyperalgesia. Findings revealed that 1) allodynia and hyperalgesia developed following UVB irradiation, 2) heat stimulation of the UVB-irradiated skin enlarged both hyperalgesic and allodynic areas (P < 0.01), and 3) muscle sensitization did not influence the effect of UVB on allodynia or the response to heat rekindling. These data suggest that heat rekindling applied to an UVB-sensitized skin can maintain or facilitate allodynia and hyperalgesia for a longer period offering a suitable model for testing analgesic compounds when sufficient duration of time is needed for investigation of drug efficacy.

Background and aims The ultraviolet-B (UVB) inflammatory model is a well-established model of inflammatory pain. This study investigated whether UVB-induced cutaneous inflammation would enhance pain responses from the underlying deep somatic areas. Methods Skin inflammation was induced, in 24 healthy volunteers, by UVB irradiation (three times of the individual minimal erythema UVB dose) in square-shaped areas on the forearm and lower back. Assessments of cutaneous blood flow, pin-prick thresholds, pressure pain thresholds and tolerance, stimulus-response functions relating graded pressure stimulations and pain intensity (visual analogue scale, VAS) were performed within and outside the irradiated area. Results Twenty-four hours after UVB irradiation, a significant increase in superficial blood flow in the irradiated skin area was demonstrated compared with baseline (P < 0.01) indicating that inflammation was induced. Compared with baseline, UVB irradiation significantly reduced the pin-prick thresholds, pressure pain thresholds and tolerance within and outside of the irradiated area (P < 0.05). The stimulus-response function was left-shifted compared with baseline both within and outside the irradiated area (P < 0.05) with a more pronounced left-shift within the irradiated area (P < 0.01). Application of topical anaesthesia 24h after irradiation in 5 subjects, both within and outside the irradiated area, could only increase the pin-prick thresholds outside the irradiated area. Conclusion The UVB irradiation of the skin not only provokes cutaneous primary and secondary hyper-algesia but also causes hyperalgesia to blunt pressure stimulations 24h after the UVB exposure. Implications The presented UVB model can be used as a translational model from animals into healthy subjects. This model can potentially be used to screen drug candidates with anti-inflammatory properties in early stages of drug development.