Wang Xiaolin, Li Jinqing, Li Liwen, Li Xueyong
Clin Lab. 2015;61(9):1257-66. doi: 10.7754/clin.lab.2015.150222.
It has been demonstrated that photodynamic therapy (PDT) is a promising treatment approach for hyperplastic dermatosis and results in a beneficial outcome. In the present study, PDT involving hematoporphyrin monomethyl ether (HMME) was applied to keloid fibroblasts (KFB), and the effects and the mechanism of action were explored.
Keloid fibroblastic cells were divided into four groups (PDT group, light alone group, HMME alone group, normal cultured group). Cell proliferation and apoptosis were observed. Radical oxygen species (ROS) were detected by means of dihydroethidium (DHE) and dihydrorhodamine (DHR123). ROS in the PDT group were also assessed after addition of tiron.
Cell proliferation was inhibited in the PDT group (p < 0.05), while the rate of apoptosis was also clearly increased (p < 0.05). The levels of ROS were significantly higher in the PDT group than was observed in the other three groups (p < 0.05). With the addition of tiron the damaging effects were reduced.
Our data indicated that HMME-mediated PDT could inhibit keloid fibroblast proliferation and could also induce apoptosis. This process was associated with the production of ROS.
已证实光动力疗法（PDT）是增生性皮肤病一种有前景的治疗方法，且疗效良好。在本研究中，将含单甲醚血卟啉（HMME）的光动力疗法应用于瘢痕疙瘩成纤维细胞（KFB），并探究其效果及作用机制。
将瘢痕疙瘩成纤维细胞分为四组（光动力疗法组、单纯光照组、单纯HMME组、正常培养组）。观察细胞增殖和凋亡情况。通过二氢乙锭（DHE）和二氢罗丹明（DHR123）检测活性氧（ROS）。在加入替诺后也评估了光动力疗法组中的ROS。
光动力疗法组细胞增殖受到抑制（p < 0.05），同时凋亡率也明显升高（p < 0.05）。光动力疗法组中的ROS水平显著高于其他三组（p < 0.05）。加入替诺后，损伤作用降低。
我们的数据表明，HMME介导的光动力疗法可抑制瘢痕疙瘩成纤维细胞增殖，还可诱导凋亡。这一过程与ROS的产生有关。
