Hinokitiol, an iron chelator originally extracted from woods of Thuja plicata and Chamaecyparis obtuse, has been found to inhibit ultraviolet B-induced apoptosis in keratinocytes of murine ear skin via antioxidant activity of metallothionein. It can partially mimic the function of missing protein transporters of iron, and possibly other ions, may have potential in treating human diseases.
Hinokitiol, a tropolone-related natural compound, is known to induce apoptosis and cell cycle arrest and has anti-inflammatory and anti-tumor activities. Hinokitiol may exert DNA demethylation by inhibiting the expression of DNMT1 (DNA methyltransferase 1) and UHRF1 (RING finger domain 1) in colon cancer cells[3]. In U87MG and T98G glioma cell lines, hinokitiol demonstrates a dose-dependent decrease in viability, with IC50 values of 316.5 ± 35.5 and 152.5 ± 25.3 µM, respectively. Hinokitiol represses ALDH activity and self-renewal ability in glioma stem cells, and inhibits in vitro oncogenicity. Hinokitiol also reduces Nrf2 expression in glioma stem cells in a dose-dependent manner[4]. Hinokitiol attenuates liver injury following HS/R (Haemorrhagic shock and resuscitation), partly through the inhibition of NF-κB activation[5]. Moreover, hinokitiol inhibited the migration of lung cancer A549 cells through several mechanisms, including the activation of caspases-9 and -3, induction of p53/Bax and antioxidant CAT (antioxidant enzymes catalase) and SOD (superoxide dismutase), and reduction of MMP-2 and -9 (matrix metalloproteinases) activities. It also induces cytochrome c expression[6].
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