摘要
目的探讨压力疗法对烧伤患者增生性瘢痕(HS)中细胞增殖亡的影响,方法笔街尊位2010年9月-2012年9月收治的20例患者,深Ⅱ~Ⅲ度烧伤创向愈合后2周(HS形成初期)开始,每天穿戴由笔者单位康复医师跹身定做的压力衣20h以上,将其设为压力治疗组。另将笔者单位同期收治的深Ⅱ~Ⅲ度烧伤后HS形成3、6、12、24个月未接受任治疗的患者各5例,设为对照组。取压力治疗组治疗后3、6、12、24个月瘢痕切除植皮术中切除弃用的四肢、面部等处HS组织(每个时相点5例患者),取对照组患者入院后2~3d瘢痕切除植皮术中切除弁用的四肢、面部等处HS组织。按照随机数字农法选取前述40例患者中5例患者,取其术中弃用的腹部及大腿正常皮肤组织作为止常对照。采用免疫组织化学染色法检测HS及正常皮肤组织中增殖细胞核抗原(PCNA)的表达,原位末端标记法检测细胞凋亡:情况,实时荧光定量PCR法检测P57^kip2和细胞周期蛋白E的mRNA表达。对数据进行t检验、单因素方筹分析或LSD检验。结果(1)在正常皮肤组织中,仅可于表皮基底层及棘细胞层见PCNA阳性细胞;压力治疗组和对照组可于HS表皮基底层、棘细胞层、颗粒细胞层中下部及真皮中见到PCN阳性细胞。压力治疗组治疗后3、6、12个月HS中PCNA阳性细胞百分比分别勾(40.4±2.9)%、(28.2±6.2)%、(9.9±0.7)%,明显低下对照纰形成3、6、12个月HS中的(48.3±4.7)%、(36,2±3.2)%、(11.4±0.9)%(t值分别为3.186、2.559、2.880,P价均小于0.05)。(2)在正常皮肤组织中,仅可于表皮雎底细胞层见凋亡细胞;压力治疗绀及对照组HS表皮各层均可见捌亡细胞。压力治疗组治疗后6、12、24个月HS中凋亡指数分别为(20.4±1.2)%、(26.1±0.4)%、(26.6±1.0)%,明显高于对照绀形成6、12、24个川Hs的(16.2±1.5)%、(23.1±2.0)%、(24.8±J.1)%(t值分另Ⅱ为一4.904、一3.366、一2.606,,】〈0.05或P〈0.01)。(3)ni力治疗组治疗后3、6、12个月HS中P57kli,2mRNA的表达节分别为3.87±0.20、8.60±0.78、10.00±0.57,明显高j:对照组肜成3、6、12个川HS的3.34±0.15、6.36±0.29、9.34±0.12(t值分刖为一4.880、一6.014、一2.375,P〈0.05或P〈0.01)。正常皮肤组织P57kip2mRNA表达量与压力治疗绀治疗后12、24个月及对照组形成12、24个月HS中P57^kip2 mRNA农达髓相近(P觚均大于0.05).,(4)压力治疗组治疗后3、6、12个川HS中细胞删期货白EtuRNA的表达量分别为19.30±0.18、12.77±0.30、9.2l±0.18,明显低于对照组形成3、6、12个月HS的19.79±0.34、154l±0.26、9.47±0.17(t值分别为3.186、2.559、2.880,P〈0.05或P〈0.01)。正常皮肷绀织绌胞圳期篮白EmRNA我达堪与压力治疗组治疗后12、24个月及对照组肜成12、24个JJIIsLfJ细胞川期蚩白EtuRNA表达最相近(P值均大于0.05)。结论压力疗法能通过有效抑制HS中细胞增殖同时促进其凋亡,从而加速HS的演变进程,起到抑制瘢痕增生的目的.
Objective To explore the effects of pressure therapy on proliferation and apoptosis uf ceils in hypertrophic scar (HS) of burn patients. Methods Twenty patients who were hospitalized from September 2010 to September 2012 and started to wear pressure garment tailored by rehabilitation therapists over 20 hours a day beginning from two weeks after healing of burn wounds with the depth from deep partial- thickness to full-thickness (early stage of formation of HS) were set as pressure treatment group (PT). An- other group of patients who were hospitalized in the same period with HS formed 3, 6, 12, 24 months ( with 5 patients at each time point) after deep partial-thickness to full-thickness burns without receiving any treat- ment were set as control group. HS tissue samples from limbs and face were excised at post treatment month (PTM) 3, 6, 12, 24 in group PT (with 5 patients at each time point), and 2 to 3 days after admission in control group. Five patients out of the above-mentioned 40 patients were selected according to the random number table, and normal skin tissue samples from abdomen and thigh were also obtained to serve as normal control. The expressions of proliferating cell nuclear antigen (PCNA) in HS and normal skin tissue were de- termined with immunohistochemical staining. The apoptosis status was detected with situ end labeling tech- nique. The mRNA expressions of P57klp2 and Cyclin E were determined with real-time fluorescence quantifi- cation PCR. Data were processed with t test, one-way analysis of variance, or LSD test. Results ( 1 ) In normal skin tissue, PCNA-positive cells were observed in the epidermal basal layer and prickle cell layer. In group PT and control group, PCNA-positive cells were observed in the epidermal basal layer, prickle cell lay- er, lower part of the granular cell layer, and dermis of HS. The percentages of PCNA-positive cells in HS in group PT were respectively (40.4 +2.9)%, (28.2 +6.2)%, (9.9 "+0.7)% at PTM3, 6, 12, which were significantly lower than those of HS formed 3, 6, 12 months after wound healing in control group [ (48.3 "+ 4.7)%, (36.2_+3.2)%, (11.4+0.9)%, with t values respectively3.186, 2. 559, 2. 880, P values all below 0. 05 ~. (2) In normal skin tissue, apoptotic cells were observed in the epidermal basal layer, in group PT and control group, apoptotic cells were observed in each layer of epidermis of HS. The apoptotic indexes of HS in group PT were respectively (20.4 _+ 1.2)% , (26.1 -+0.4)% , (26.6 "+ 1.0)% at PTM 6, 12, 24, which were significantly higher than those of HS formed 6, 12, 24 months after wound healing in control group [(16.2+ 1.5)%, (23. 1 _+2.0)%, (24.8 + 1. 1)%, with t values respectively -4.904, -3.366, -2. 606, P 〈0.05 orP 〈0.01]. (3) The mRNA expressions of P57kip2 of HS in group PT were respec- tively 3.87 -+ 0.20, 8.60 "+ 0.78, 10.00 -+ 0.57 at PTM 3, 6, 12, which were significantly higher than those of HS formed 3, 6, 12 months after wound healing in control group (3.34 -+0.15, 6.36 -+0.29, 9.34 +0.12, with t values respectively -4.880, -6.014, -2.375,P 〈0.05 orP 〈0.01). The mRNA expression of P57klp2 in normal skin tissue was close to those of HS in group PT at PTM 12, 24 and those of HS formed 12, 24 months after wound healing in control group (with P values all above 0.05 ). (4) The mRNA expressions of Cyclin E of HS in group PT were respectively 19.30 "+0.18, 12.77 +0.30, 9.21 -+0.18 at PTM 3, 6, 12, which were significantly higher than those of HS formed 3, 6, 12 months after wound healing in control group ( 19.79 + 0.34, 15.41 -+ 0.26, 9.47 "+ 0.17, with t values respectively 3. 186, 2. 559, 2. 880, P 〈 0.05 or P 〈0.01). The mRNA expression of Cyclin E in normal skin tissue was close to those of HS in group PT at PTM 12, 24 and those of HS formed 12, 24 months after wound healing in control group (with P values all above 0.05 ). Conclusions Pressure therapy can accelerate the evolution process of HS through accelerating apoptosis and inhibition of cell proliferation, thereby scar proliferation is inhibited.
出处
《中华烧伤杂志》
CAS
CSCD
北大核心
2013年第6期509-515,共7页
Chinese Journal of Burns
基金
云南省卫生科技计划项目(2010NS065)
关键词
烧伤
细胞增殖
细胞凋亡
增生性瘢痕
压力疗法
Burns
Cell proliferation
Apoptosis
Hypertrophic scar
Pressure therapy