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

Analyze the expression of Bax and Caspase-3 in epidermal keratinocytes of chronic UV-damaged mice

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。

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.