中华烧伤杂志
中華燒傷雜誌
중화소상잡지
16
2011年
6期
416-421
,共6页
支燕%付晋凤%袁卫红%陈斌%李玲%危群%佟颖
支燕%付晉鳳%袁衛紅%陳斌%李玲%危群%佟穎
지연%부진봉%원위홍%진빈%리령%위군%동영
放射性同位素%瘢痕%成纤维细胞%细胞周期
放射性同位素%瘢痕%成纖維細胞%細胞週期
방사성동위소%반흔%성섬유세포%세포주기
Radioisotopes%Cicatrix%Fibroblasts%Cell cycle%Apoptosis%Collagen type Ⅰ
目的 探讨90Sr防治瘢痕增生的作用机制并观察临床疗效. 方法 用90Sr敷贴器按照0、5、10,15 Gy剂量照射体外培养的人增生性瘢痕Fb.照射后24、48、72 h,流式细胞仪测定细胞周期及凋亡率变化,ELISA法检测细胞培养上清液中Ⅰ型腔原浓度.评价348例增生性瘢痕患者、40例瘢痕疙瘩患者及114例外科手术后瘢痕预防患者应用90Sr照射治疗的效果,并经HE染色对比正常皮肤组织、增生性瘢痕组织、经90SR照射治疗的增生性瘢痕组织中Fb数目.对数据进行单因素方差分析和q检验. 结果 (1)剂量为10、15 Gy的90Sr照射后24、48 h,细胞凋亡率呈逐渐上升趋势,至照射后72 h两者凋亡率相近.剂量为5 Gy的90Sr照射后48 h细胞凋亡率明显高于照射后24 h,但照射后72 h细胞凋亡率迅速下降,与剂量为10、15 Gy时比较差异均有统计学意义(F值均为916.711,P值均小于0.01).(2)照射后24h,90Sr照射剂量为5、10 Gy时,细胞各周期的百分比相近；90Sr照射剂量为15 Gy时,S期细胞明显增多[(48.1±1.0)％,F值均为200.277,P值均小于0.01].剂量为10 Gy及15 Gy的90Sr照射后72 h,细胞明显阻滞在S期,S期细胞百分比分别为(85.7±5.2)％、(73.0±8.4)％,与照射剂量为0 Gy和5 Gy时比较差异均有统计学意义(F值均为111.105,P值均小于0.01).(3)同一照射时相点下,照射剂量越大,Ⅰ型胶原浓度越低(F值为5044.449～8234.423,P值均小于0.01).同一照射剂量下,随着时间推移,Ⅰ型胶原浓度有不同程度的增加(F值为333.395～2973.730,P值均小于0.01).(4)临床病例观察显示,90Sr照射病理性瘢痕或术后瘢痕预防患者后,显效率及有效率累计88.45％.HE染色显示,90Sr照射治疗的人增生性瘢痕Fb数目[每200倍视野(86±20)个]少于未经照射治疗者[每200倍视野(198±65)个,F=208.405,P＜0.05]. 结论 90Sr抑制瘢痕的生长是其对瘢痕Fb和ECM共同作用的结果,且临床疗效显著.
目的 探討90Sr防治瘢痕增生的作用機製併觀察臨床療效. 方法 用90Sr敷貼器按照0、5、10,15 Gy劑量照射體外培養的人增生性瘢痕Fb.照射後24、48、72 h,流式細胞儀測定細胞週期及凋亡率變化,ELISA法檢測細胞培養上清液中Ⅰ型腔原濃度.評價348例增生性瘢痕患者、40例瘢痕疙瘩患者及114例外科手術後瘢痕預防患者應用90Sr照射治療的效果,併經HE染色對比正常皮膚組織、增生性瘢痕組織、經90SR照射治療的增生性瘢痕組織中Fb數目.對數據進行單因素方差分析和q檢驗. 結果 (1)劑量為10、15 Gy的90Sr照射後24、48 h,細胞凋亡率呈逐漸上升趨勢,至照射後72 h兩者凋亡率相近.劑量為5 Gy的90Sr照射後48 h細胞凋亡率明顯高于照射後24 h,但照射後72 h細胞凋亡率迅速下降,與劑量為10、15 Gy時比較差異均有統計學意義(F值均為916.711,P值均小于0.01).(2)照射後24h,90Sr照射劑量為5、10 Gy時,細胞各週期的百分比相近；90Sr照射劑量為15 Gy時,S期細胞明顯增多[(48.1±1.0)％,F值均為200.277,P值均小于0.01].劑量為10 Gy及15 Gy的90Sr照射後72 h,細胞明顯阻滯在S期,S期細胞百分比分彆為(85.7±5.2)％、(73.0±8.4)％,與照射劑量為0 Gy和5 Gy時比較差異均有統計學意義(F值均為111.105,P值均小于0.01).(3)同一照射時相點下,照射劑量越大,Ⅰ型膠原濃度越低(F值為5044.449～8234.423,P值均小于0.01).同一照射劑量下,隨著時間推移,Ⅰ型膠原濃度有不同程度的增加(F值為333.395～2973.730,P值均小于0.01).(4)臨床病例觀察顯示,90Sr照射病理性瘢痕或術後瘢痕預防患者後,顯效率及有效率纍計88.45％.HE染色顯示,90Sr照射治療的人增生性瘢痕Fb數目[每200倍視野(86±20)箇]少于未經照射治療者[每200倍視野(198±65)箇,F=208.405,P＜0.05]. 結論 90Sr抑製瘢痕的生長是其對瘢痕Fb和ECM共同作用的結果,且臨床療效顯著.
목적 탐토90Sr방치반흔증생적작용궤제병관찰림상료효. 방법 용90Sr부첩기안조0、5、10,15 Gy제량조사체외배양적인증생성반흔Fb.조사후24、48、72 h,류식세포의측정세포주기급조망솔변화,ELISA법검측세포배양상청액중Ⅰ형강원농도.평개348례증생성반흔환자、40례반흔흘탑환자급114예외과수술후반흔예방환자응용90Sr조사치료적효과,병경HE염색대비정상피부조직、증생성반흔조직、경90SR조사치료적증생성반흔조직중Fb수목.대수거진행단인소방차분석화q검험. 결과 (1)제량위10、15 Gy적90Sr조사후24、48 h,세포조망솔정축점상승추세,지조사후72 h량자조망솔상근.제량위5 Gy적90Sr조사후48 h세포조망솔명현고우조사후24 h,단조사후72 h세포조망솔신속하강,여제량위10、15 Gy시비교차이균유통계학의의(F치균위916.711,P치균소우0.01).(2)조사후24h,90Sr조사제량위5、10 Gy시,세포각주기적백분비상근；90Sr조사제량위15 Gy시,S기세포명현증다[(48.1±1.0)％,F치균위200.277,P치균소우0.01].제량위10 Gy급15 Gy적90Sr조사후72 h,세포명현조체재S기,S기세포백분비분별위(85.7±5.2)％、(73.0±8.4)％,여조사제량위0 Gy화5 Gy시비교차이균유통계학의의(F치균위111.105,P치균소우0.01).(3)동일조사시상점하,조사제량월대,Ⅰ형효원농도월저(F치위5044.449～8234.423,P치균소우0.01).동일조사제량하,수착시간추이,Ⅰ형효원농도유불동정도적증가(F치위333.395～2973.730,P치균소우0.01).(4)림상병례관찰현시,90Sr조사병이성반흔혹술후반흔예방환자후,현효솔급유효솔루계88.45％.HE염색현시,90Sr조사치료적인증생성반흔Fb수목[매200배시야(86±20)개]소우미경조사치료자[매200배시야(198±65)개,F=208.405,P＜0.05]. 결론 90Sr억제반흔적생장시기대반흔Fb화ECM공동작용적결과,차림상료효현저.
Objective To analyze the potential mechanism of preventive and therapeutic effects of 90Sr on hypertrophic scar,and to observe its clinical effect.Methods Fibroblasts isolated from human hypertrophic scar were cultured in vitro and radiated by 90Sr 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 90Sr 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 90Sr radiation.Data were processed with one-way analysis of variance and q test,Results (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 90Sr radiation (86 ± 20) was less than that in patients without treatment [ ( 198 ± 65 ),F =208.405,P ＜ 0.05]. Conclusions The effect of 90 Sr radiation on fibroblasts and extracellular matrix can contribute to inhibition of scar formation,and the clinical effect is.significant.
