Inhibitory effect of beta-thujaplicin on ultraviolet B-induced apoptosis in mouse keratinocytes.
Inhibitory effect of beta-thujaplicin on ultraviolet B-induced apoptosis in mouse keratinocytes.
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β-thujaplicin 对紫外线 B 诱导的小鼠角质形成细胞凋亡的抑制作用。
DOI：
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发表时间：
1998
影响因子：
6.5
通讯作者：
Yaeno Arima
中科院分区：
文献类型：
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作者：
T. Baba;H. Nakano;K. Tamai;D. Sawamura;K. Hanada;I. Hashimoto;Yaeno Arima
晒伤细胞被认为是紫外线b诱导的角化细胞凋亡。研究表明，酶促和非酶促抗氧化剂可有效抑制晒伤细胞的形成，这表明活性氧可能在紫外线b诱导的细胞凋亡过程中发挥作用。金属硫蛋白是一种细胞质蛋白，具有抗氧化活性，据报道，金属硫蛋白的过度表达可以减少小鼠皮肤中晒伤细胞的数量。我们也证明过表达金属硫蛋白抑制紫外线b诱导的小鼠角化细胞DNA阶梯形成。这些发现支持了细胞金属硫蛋白可能通过其抗氧化活性在抑制紫外线b诱导的角质形成细胞凋亡中发挥重要作用的假设。本研究主要研究了胡贾木提取物β -胡贾木苷的药理作用。和chamacyparis钝，Sieb。调查。紫外线b诱导角质形成细胞凋亡和金属硫蛋白诱导。局部应用β -图贾普林可减少小鼠耳皮肤中紫外线b介导的晒伤细胞和末端脱氧核苷酸转移酶（TdT）介导的dutp -生物素缺口末端标记阳性细胞的数量。β -thujaplicin抑制紫外线b诱导的小鼠角化细胞DNA阶梯形成。组织化学分析表明，局部应用β -土豆杉素可诱导小鼠皮肤中金属硫蛋白的表达。Northern分析和western blotting显示，在β -thujaplicin处理的培养小鼠角质形成细胞中，金属硫蛋白mRNA和金属硫蛋白分别被显著诱导。这些结果表明，β -thujaplicin抑制紫外线b诱导的角化细胞凋亡，并强烈提示其抑制机制是由于该药物诱导金属硫蛋白的抗氧化活性所致。
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.