低频超声激活光敏剂ATX-S10和HPD的实验研究

目的:对比低频超声条件下不同体积、不同浓度的ATX-S10和HPD的单态氧的荧光,探讨二者的声激活程度。方法:以17 KHz换能器作为辐射声源,利用光电倍增管收集单态氧的荧光强度,对比不同体积、浓度时ATX-S10和HPD的激活程度。结果:(1)在405 nm处,不同声功率的相对荧光强度在声致发光出现最大值前呈现平缓的阶梯变化趋势,超过60 W后,声致发光迅速增加至4~5倍,到达最大值后迅速下降。(2)相同体积的ATX-S10的荧光强度均比HPD高。同种光敏剂在不同浓度下,出现饱和趋势的体积相同,HPD样品体积大于5 mL,ATX-S10大于6 mL,荧光强度的增加趋势变缓,达到饱和。(3)ATX-S10和HPD在1270 nm附近的荧光强度随浓度的变化逐渐最大,呈近似的线性变化。结论:辐射强度越高,单态氧产量高,激活程度高,浓度越高,激活程度高。相同条件下光敏剂ATX-S10的单态氧产率比HPD高。

Early apoptosis and cell death induced by ATX-S10Na(Ⅱ)-mediated photodynamic therapy are Bax- and p53-dependent in human colon cancer cells

AIM： To investigate the roles of Bax and p53 proteins in photosensitivity of human colon cancer cells by using lysosome-localizing photosensitizer, ATX-S10Na （Ⅱ）. METHODS： HCT116 human colon cancer cells and Bax-null or p53-null isogenic derivatives were irradiated with a diode laser. Early apoptosis and cell death in response to photodynamic therapy were determined by MTT assays, annexin Ⅴ assays, transmission electron microscopy assays, caspase assays and western blotting. RESULTS： Induction of early apoptosis and cell death was Bax- and p53-dependent. Bax and p53 were required for caspase-dependent apoptosis. The levels of anti-apoptotic Bcl-2 family proteins, Bcl-2 and Bcl-xL, were decreased in Bax- and p53-independent manner. CONCLUSION： Our results indicate that eady apoptosis and cell death of human colon cancer cells induced by photodynamic therapy with lysosome-localizing photosensitizer ATX-S10Na （Ⅱ） are mediated by p53- Bax network and low levels of Bcl-2 and Bcl-xL proteins. Our results might help in formulating new therapeutic approaches in photodynamic therapy.