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慢性紫外线损伤小鼠模型皮肤角质形成细胞中Bax和Caspase-3的表达
  • 期刊名称:中国皮肤性病学杂志
  • 时间:0
  • 页码:22-26
  • 语言:中文
  • 分类:R75[医药卫生—皮肤病学与性病学;医药卫生—临床医学]
  • 作者机构:[1]天津医科大学总医院,天津300052, [2]中国医学科学院北京协和医学院皮肤病研究所,江苏南京210042
  • 相关基金:国家自然科学基金(编号:30872268);天津市卫生局科技基金(编号:09KZ52);江苏省基础研究计划(自然科学基金)画上项目(BK2010135)
  • 相关项目:自噬与人皮肤成纤维细胞光老化关系及相关信号调节的研究
中文摘要:

目的观察对照组小鼠与慢性紫外线(Ultraviolet,UV)损伤组小鼠背部皮肤组织角质形成细胞中凋亡相关蛋白(Bax)与半胱氨酸天冬氨酸蛋白酶-3(Caspase-3)的表达情况,分析UV对小鼠慢性UV损伤中两指标表达变化的生物学意义。方法应用UV治疗仪对实验小鼠进行照射,建立慢性UV损伤小鼠模型,应用免疫组化PV二步法检测UV照光前、后小鼠皮肤角质形成细胞中Bax和Caspase-3表达的变化情况并进行对比。结果对照组小鼠实验前Bax和Caspase-3阳性率分别为30%和20%,实验后均为30%,差异均无统计学意义(P均〉0.05)。慢性UV损伤组小鼠实验前Bax和Caspase-3阳性率分别为30%和20%,实验后均为100%,慢性UV损伤组小鼠显著高于对照组,且实验前、后两者差异均有统计学意义(P均〈0.05)。造模后慢性UV损伤组小鼠表皮角质形成细胞内的Bax和Csapase-3的表达水平均明显增加,且二者增加程度有相关性(r=0.487,P〈0.05)。结论重复UV照射可以诱导小鼠表皮角质形成细胞中Caspase-3表达上调和凋亡活性上升,且这种凋亡活性的上升与Bax的表达上调密切相关。

英文摘要:

Objective To observe the expression of Bax and Caspase-3 in epidermal keratinocytes of the back skin, form mice of control group and chronic UV-damaged group, and analyze the biological meaning of UV for the changed expression of the two indicators in the experiment of chronic UV-damaged mice. Methods Estab- lish the model of chronic UV-damaged mice by exposing mice under the UV light, then contrase the change of Bax and Caspase-3 by imtnunohistochemistry, in epidermal keratinocytes, both before and after exposion under UV light. Results The positive rate of Bax and Caspase-3 in control group were 30% and 20% be- fore the experiment and similer with 30% and 30% after the UV light exposion. There was no statistical sig- nificance between the two groups (P 〉0, 05). The positive rate of Bax and Caspase-3 in chronic UV-dam- aged mice were 30% and 20% before the experiment and 100% and 100% after the UV light exposion. The expression of Bax and Caspase-3 in chronic UV-damaged mice was higher than that in the control group. The difference between groups had statistical meaning (P 〈 0.05 ), and increase of the two indicators had corre- lation (r =0. 487,P 〈 0.05). Conclusion Repeated UV light can induce upregulation of Caspase-3 and increase its apoptotic activity of epidermal keratinocytes in mice. And the increase of apoptotic activity is re- lated with the increased exnression of Bax.

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