Zhi Yan, Fu Jin-feng, Yuan Wei-hong, Chen Bin, Li Ling, Wei Qun, Tong Ying
Department of Burns, Burn Institute of Yunnan Province, Kunming, China.
Zhonghua Shao Shang Za Zhi. 2011 Dec;27(6):416-21.
To analyze the potential mechanism of preventive and therapeutic effects of (90)Sr on hypertrophic scar, and to observe its clinical effect.
Fibroblasts isolated from human hypertrophic scar were cultured in vitro and radiated by (90)Sr with the dose varying from 0 Gy (control group) to 5 Gy (LD group), 10 Gy (MD group), and 15 Gy (HD group). The cell cycle and apoptosis rate were determined by flow cytometry at post radiation hour (PRH) 24, 48, and 72. The concentration of type I collagen in cell supernatant was detected by enzyme-linked immunosorbent assay (ELISA). Therapeutic effects of (90)Sr radiation were evaluated among 348 patients with hypertrophic scars, 40 patients with keloids, and 114 patients for scar prevention after surgical operation. The number of fibroblasts after HE staining was compared among normal skin tissue, hypertrophic scar, and hypertrophic scar treated with (90)Sr radiation. Data were processed with one-way analysis of variance and q test.
(1) Apoptotic rates in MD and HD groups at PRH 48 were higher than those at PRH 24, and the apoptotic rate was similar between MD group and HD group at PRH 72. Apoptotic rate in LD group at PRH 48 was significantly higher than that at PRH 24, but it decreased rapidly at PRH 72, which was significantly lower than those in MD and HD groups (with F values all equal to 916.711, P values all below 0.01). (2) At PRH 24, cell ratios of each phase in LD and HD groups were similar, and cell ratio of S phase in HD group [(48.1 ± 1.0)%] was higher than those in the other three groups (with F values all equal to 200.277, P values all below 0.01). At PRH 72, cell ratio of S phase in MD and HD groups was respectively (85.7 ± 5.2)%, (73.0 ± 8.4)%, implying that cells were blocked in S phase, and the values were all higher than those in control and LD groups (with F values all equal to 111.105, P values all below 0.01). (3) At the same time point, the concentration of type I collagen decreased along with the increase of radiation dose (with F values from 5044.449 to 8234.432, P values all below 0.01). With the same radiation dose, the concentration of type I collagen increased along with prolongation of time (with F values from 333.395 to 2973.730, P values all below 0.01). (4) Clinical observation showed the (obvious) effective rate of radiation for pathological scars and that for scar prevention after surgical operation added up to 88.45%. The number of fibroblasts per 200 times visual field in patients after (90)Sr radiation (86 ± 20) was less than that in patients without treatment [(198 ± 65), F = 208.405, P < 0.05].
The effect of (90)Sr radiation on fibroblasts and extracellular matrix can contribute to inhibition of scar formation, and the clinical effect is significant.
分析⁹⁰Sr对增生性瘢痕防治作用的潜在机制，并观察其临床效果。
将人增生性瘢痕分离出的成纤维细胞进行体外培养，分别用0 Gy（对照组）、5 Gy（低剂量组）、10 Gy（中剂量组）和15 Gy（高剂量组）的⁹⁰Sr进行照射。于照射后24、48和72小时，采用流式细胞术检测细胞周期和凋亡率。采用酶联免疫吸附测定法（ELISA）检测细胞上清液中Ⅰ型胶原的浓度。对348例增生性瘢痕患者、40例瘢痕疙瘩患者及114例术后瘢痕预防患者进行⁹⁰Sr照射治疗效果评估。比较正常皮肤组织、增生性瘢痕及经⁹⁰Sr照射的增生性瘢痕组织经HE染色后的成纤维细胞数量。数据采用单因素方差分析和q检验进行处理。
（1）中剂量组和高剂量组照射后48小时的凋亡率高于照射后24小时，照射后72小时中剂量组和高剂量组的凋亡率相近。低剂量组照射后48小时的凋亡率显著高于照射后24小时，但在照射后72小时迅速下降，显著低于中剂量组和高剂量组（F值均为916.711，P值均小于0.01）。（2）照射后24小时，低剂量组和高剂量组各时相细胞比例相近，高剂量组S期细胞比例为（48.1±1.0）%，高于其他三组（F值均为200.277，P值均小于0.01）。照射后72小时，中剂量组和高剂量组S期细胞比例分别为（85.7±5.2）%、（73.0±8.4）%，提示细胞阻滞于S期，且均高于对照组和低剂量组（F值均为111.105，P值均小于0.01）。（3）同一时间点，Ⅰ型胶原浓度随照射剂量增加而降低（F值为5044.449～8234.432，P值均小于0.01）。相同照射剂量下，Ⅰ型胶原浓度随时间延长而升高（F值为333.395～2973.730，P值均小于0.01）。（4）临床观察显示，⁹⁰Sr照射对病理性瘢痕及术后瘢痕预防的总有效率为88.45%。⁹⁰Sr照射患者每200视野成纤维细胞数为（86±20）个，少于未治疗患者[（198±65）个，F = 208.405，P < 0.05]。
⁹⁰Sr照射对成纤维细胞和细胞外基质的作用有助于抑制瘢痕形成，临床效果显著。
