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Inhibitory effect of beta-thujaplicin on ultraviolet B-induced apoptosis in mouse keratinocytes
1Department of Dermatology, Hirosaki University School of Medicine, Japan.
Abstract:
Sunburn cells are thought to represent ultraviolet B-induced apoptotic keratinocytes. It has been demonstrated that enzymatic and nonenzymatic antioxidants effectively suppress sunburn cell formation, indicating that reactive oxygen species may play a role in the progression of ultraviolet B-induced apoptosis. Metallothionein, a cytosol protein, has antioxidant activity, and overexpression of metallothionein has been reported to reduce the number of sunburn cells in mouse skin. We have also demonstrated that overexpression of metallothionein inhibits ultraviolet B-induced DNA ladder formation in mouse keratinocytes. These findings support the hypothesis that cellular metallothionein may play an important role in the inhibition of ultraviolet B-induced apoptosis in keratinocytes through its antioxidant activity. In the present study, we investigated the effects of beta-thujaplicin, an extract from the woods of Thuja plicata D. Don. and Chamaecyparis obtuse, Sieb. et Zucc., on ultraviolet B-induced apoptosis in keratinocytes and on metallothionein induction. Topical application of beta-thujaplicin decreased the number of ultraviolet B-mediated sunburn cells and terminal deoxynucleotidyl transferase (TdT)-mediated dUTP-biotin nick end labeling-positive cells in mouse ear skin. Incubation with beta-thujaplicin suppressed ultraviolet B-induced DNA ladder formation in cultured mouse keratinocytes. Histochemical analysis showed that topical application of beta-thujaplicin induced metallothionein protein in mouse skin. Northern analysis and western blotting revealed significant induction of metallothionein mRNA and metallothionein protein, respectively, in beta-thujaplicin-treated cultured mouse keratinocytes. These findings indicate that beta-thujaplicin inhibits ultraviolet B-induced apoptosis in keratinocytes and strongly suggest that the inhibitory mechanism is due to the antioxidant activity of metallothionein induced by the agent.
Insights
Beta-thujaplicin, a natural extract, reduces sunburn cells by inducing metallothionein. This suggests a new approach to preventing ultraviolet B-induced skin cell apoptosis through antioxidant activity.
Area of Science:
- Dermatology
- Molecular Biology
- Biochemistry
Background:
- Sunburn cells are linked to ultraviolet B (UVB) radiation-induced keratinocyte apoptosis.
- Antioxidants can reduce sunburn cell formation, implicating reactive oxygen species in UVB-induced apoptosis.
- Metallothionein, a protein with antioxidant properties, reduces sunburn cells and DNA damage in mouse skin.
Purpose of the Study:
- To investigate the effects of beta-thujaplicin on UVB-induced apoptosis in keratinocytes.
- To determine if beta-thujaplicin can induce metallothionein production.
- To explore the role of metallothionein in beta-thujaplicin's protective effects against UVB damage.
Main Methods:
- Topical application of beta-thujaplicin on mouse ear skin.
- Assessing sunburn cells and terminal deoxynucleotidyl transferase (TdT)-mediated dUTP-biotin nick end labeling (TUNEL) positive cells.
- Investigating DNA ladder formation in cultured mouse keratinocytes.
- Histochemical analysis, Northern blotting, and Western blotting to detect metallothionein induction.
Main Results:
- Topical beta-thujaplicin significantly decreased UVB-induced sunburn cells and TUNEL-positive cells in mouse skin.
- Beta-thujaplicin suppressed UVB-induced DNA ladder formation in cultured keratinocytes.
- Histochemical, Northern, and Western blot analyses confirmed that beta-thujaplicin induced metallothionein mRNA and protein in mouse skin and keratinocytes.
Conclusions:
- Beta-thujaplicin effectively inhibits UVB-induced apoptosis in keratinocytes.
- The mechanism of inhibition involves the induction of metallothionein, leveraging its antioxidant activity.
- These findings highlight beta-thujaplicin as a potential agent for preventing UV-induced skin damage.