Hyperforin/HP-β-Cyclodextrin Enhances Mechanosensitive Ca²⁺ Signaling in HaCaT Keratinocytes and in Atopic Skin Ex Vivo Which Accelerates Wound Healing

Figure 1

The complexation of hyperforin with hydroxypropyl-β-cyclodextrin (HP--CD) and its effects on wound closure in HaCaT cells. (a) The molar ratio graph obtained by UV/Vis spectra measurements of the inclusion complex formed by hyperforin (4.66 × 10⁻⁴ M) and HP-β-CD (0–8.0 equivalents) at 25°C. (b) A possible model of the 1 : 4 complex of hyperforin/HP--CD. (c) The photodegradation of hyperforin/HP-β-CD in aqueous solution and hyperforin in methanol induced by LED light exposure. Curve fitting was performed by single exponential decay with a baseline. The baselines obtained for hyperforin/HP-β-CD and hyperforin were 44% and 1.4%, respectively. (d) The effects of hyperforin and hyperforin/HP--CD treatments on wound closure in keratinocytes under sustained stretching. Stretch stimulation (20%) facilitated wound closure in HaCaT keratinocytes (stretch). Treatment with hyperforin (1 μM) further accelerated the wound closure (stretch + hyperforin) and the wound gap was nearly closed at 6 h after scratching. Hyperforin/HP--CD (1 μM as hyperforin) showed equal or greater efficacy to hyperforin (stretch + hyperforin/HP--CD) in promoting wound closure. The data are shown as representative DIC images (upper pictures at 0 h and 6 h) and by the averages of the calculated percentage of the wound closure areas (lower graph). The quantitative data in (c) and (d) are shown as the mean ± SEM.