目的 探讨压力疗法对烧伤患者增生性瘢痕(HS)中细胞增殖与凋亡的影响. 方法 笔者单位2010年9月-2012年9月收治的20例患者,深Ⅱ~Ⅲ度烧伤创面愈合后2周(HS形成初期)开始,每天穿戴由笔者单位康复医师量身定做的压力衣20 h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个月未接受任何治疗的患者各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),取对照组患者人院后2~3d瘢痕切除植皮术中切除弃用的四肢、面部等处HS组织.按照随机数字表法选取前述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正常对照.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P57kip2和细胞周期蛋白E的mRNA表达.对数据进行t检验、单因素方差分析或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PCNA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为(40.4±2.9)%、(28.2±6.2)%、(9.9±0.7)%,明显低于对照组形成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值均小于0.05).(2)在正常皮肤组织中,仅可于表皮基底细胞层见凋亡细胞;压力治疗组及对照组HS表皮各层均可见凋亡细胞.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)%,明显高于对照组形成6、12、24个月HS的(16.2±1.5)%、(23.1 ±2.0)%、(24.8±1.1)%(t值分别为-4.904、-3.366、-2.606,P<0.05或P<0.01).(3)压力治疗组治疗后3、6、12个月HS中P57kip2mRNA的表达量分别为3.87±0.20、8.60 ±0.78、10.00±0.57,明显高于对照组形成3、6、12个月HS的3.34±0.15、6.36±0.29、9.34±0.12(t值分别为-4.880、-6.014、-2.375,P<0.05或P<0.01).正常皮肤组织P57kip2mRNA表达量与压力治疗组治疗后12、24个月及对照组形成12、24个月HS中P57kip2mRNA表达量相近(P值均大于0.05). (4)压力治疗组治疗后3、6、12个月HS中细胞周期蛋白E mRNA的表达量分别为19.30±0.18、12.77±0.30、9.21±0.18,明显低于对照组形成3、6、12个月HS的19.79±0.34、15.41±0.26、9.47±0.17(t值分别为3.186、2.559、2.880,P<0.05或P<0.01).正常皮肤组织细胞周期蛋白EmRNA表达量与压力治疗组治疗后12、24个月及对照组形成12、24个月HS中细胞周期蛋白EmRNA表达量相近(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.
目的 探討壓力療法對燒傷患者增生性瘢痕(HS)中細胞增殖與凋亡的影響. 方法 筆者單位2010年9月-2012年9月收治的20例患者,深Ⅱ~Ⅲ度燒傷創麵愈閤後2週(HS形成初期)開始,每天穿戴由筆者單位康複醫師量身定做的壓力衣20 h以上,將其設為壓力治療組.另將筆者單位同期收治的深Ⅱ~Ⅲ度燒傷後HS形成3、6、12、24箇月未接受任何治療的患者各5例,設為對照組.取壓力治療組治療後3、6、12、24箇月瘢痕切除植皮術中切除棄用的四肢、麵部等處HS組織(每箇時相點5例患者),取對照組患者人院後2~3d瘢痕切除植皮術中切除棄用的四肢、麵部等處HS組織.按照隨機數字錶法選取前述40例患者中5例患者,取其術中棄用的腹部及大腿正常皮膚組織作為正常對照.採用免疫組織化學染色法檢測HS及正常皮膚組織中增殖細胞覈抗原(PCNA)的錶達,原位末耑標記法檢測細胞凋亡情況,實時熒光定量PCR法檢測P57kip2和細胞週期蛋白E的mRNA錶達.對數據進行t檢驗、單因素方差分析或LSD檢驗. 結果 (1)在正常皮膚組織中,僅可于錶皮基底層及棘細胞層見PCNA暘性細胞;壓力治療組和對照組可于HS錶皮基底層、棘細胞層、顆粒細胞層中下部及真皮中見到PCNA暘性細胞.壓力治療組治療後3、6、12箇月HS中PCNA暘性細胞百分比分彆為(40.4±2.9)%、(28.2±6.2)%、(9.9±0.7)%,明顯低于對照組形成3、6、12箇月HS中的(48.3±4.7)%、(36.2±3.2)%、(11.4±0.9)%(t值分彆為3.186、2.559、2.880,P值均小于0.05).(2)在正常皮膚組織中,僅可于錶皮基底細胞層見凋亡細胞;壓力治療組及對照組HS錶皮各層均可見凋亡細胞.壓力治療組治療後6、12、24箇月HS中凋亡指數分彆為(20.4±1.2)%、(26.1±0.4)%、(26.6±1.0)%,明顯高于對照組形成6、12、24箇月HS的(16.2±1.5)%、(23.1 ±2.0)%、(24.8±1.1)%(t值分彆為-4.904、-3.366、-2.606,P<0.05或P<0.01).(3)壓力治療組治療後3、6、12箇月HS中P57kip2mRNA的錶達量分彆為3.87±0.20、8.60 ±0.78、10.00±0.57,明顯高于對照組形成3、6、12箇月HS的3.34±0.15、6.36±0.29、9.34±0.12(t值分彆為-4.880、-6.014、-2.375,P<0.05或P<0.01).正常皮膚組織P57kip2mRNA錶達量與壓力治療組治療後12、24箇月及對照組形成12、24箇月HS中P57kip2mRNA錶達量相近(P值均大于0.05). (4)壓力治療組治療後3、6、12箇月HS中細胞週期蛋白E mRNA的錶達量分彆為19.30±0.18、12.77±0.30、9.21±0.18,明顯低于對照組形成3、6、12箇月HS的19.79±0.34、15.41±0.26、9.47±0.17(t值分彆為3.186、2.559、2.880,P<0.05或P<0.01).正常皮膚組織細胞週期蛋白EmRNA錶達量與壓力治療組治療後12、24箇月及對照組形成12、24箇月HS中細胞週期蛋白EmRNA錶達量相近(P值均大于0.05). 結論 壓力療法能通過有效抑製HS中細胞增殖同時促進其凋亡,從而加速HS的縯變進程,起到抑製瘢痕增生的目的.
목적 탐토압력요법대소상환자증생성반흔(HS)중세포증식여조망적영향. 방법 필자단위2010년9월-2012년9월수치적20례환자,심Ⅱ~Ⅲ도소상창면유합후2주(HS형성초기)개시,매천천대유필자단위강복의사량신정주적압력의20 h이상,장기설위압력치료조.령장필자단위동기수치적심Ⅱ~Ⅲ도소상후HS형성3、6、12、24개월미접수임하치료적환자각5례,설위대조조.취압력치료조치료후3、6、12、24개월반흔절제식피술중절제기용적사지、면부등처HS조직(매개시상점5례환자),취대조조환자인원후2~3d반흔절제식피술중절제기용적사지、면부등처HS조직.안조수궤수자표법선취전술40례환자중5례환자,취기술중기용적복부급대퇴정상피부조직작위정상대조.채용면역조직화학염색법검측HS급정상피부조직중증식세포핵항원(PCNA)적표체,원위말단표기법검측세포조망정황,실시형광정량PCR법검측P57kip2화세포주기단백E적mRNA표체.대수거진행t검험、단인소방차분석혹LSD검험. 결과 (1)재정상피부조직중,부가우표피기저층급극세포층견PCNA양성세포;압력치료조화대조조가우HS표피기저층、극세포층、과립세포층중하부급진피중견도PCNA양성세포.압력치료조치료후3、6、12개월HS중PCNA양성세포백분비분별위(40.4±2.9)%、(28.2±6.2)%、(9.9±0.7)%,명현저우대조조형성3、6、12개월HS중적(48.3±4.7)%、(36.2±3.2)%、(11.4±0.9)%(t치분별위3.186、2.559、2.880,P치균소우0.05).(2)재정상피부조직중,부가우표피기저세포층견조망세포;압력치료조급대조조HS표피각층균가견조망세포.압력치료조치료후6、12、24개월HS중조망지수분별위(20.4±1.2)%、(26.1±0.4)%、(26.6±1.0)%,명현고우대조조형성6、12、24개월HS적(16.2±1.5)%、(23.1 ±2.0)%、(24.8±1.1)%(t치분별위-4.904、-3.366、-2.606,P<0.05혹P<0.01).(3)압력치료조치료후3、6、12개월HS중P57kip2mRNA적표체량분별위3.87±0.20、8.60 ±0.78、10.00±0.57,명현고우대조조형성3、6、12개월HS적3.34±0.15、6.36±0.29、9.34±0.12(t치분별위-4.880、-6.014、-2.375,P<0.05혹P<0.01).정상피부조직P57kip2mRNA표체량여압력치료조치료후12、24개월급대조조형성12、24개월HS중P57kip2mRNA표체량상근(P치균대우0.05). (4)압력치료조치료후3、6、12개월HS중세포주기단백E mRNA적표체량분별위19.30±0.18、12.77±0.30、9.21±0.18,명현저우대조조형성3、6、12개월HS적19.79±0.34、15.41±0.26、9.47±0.17(t치분별위3.186、2.559、2.880,P<0.05혹P<0.01).정상피부조직세포주기단백EmRNA표체량여압력치료조치료후12、24개월급대조조형성12、24개월HS중세포주기단백EmRNA표체량상근(P치균대우0.05). 결론 압력요법능통과유효억제HS중세포증식동시촉진기조망,종이가속HS적연변진정,기도억제반흔증생적목적.
Objective To explore the effects of pressure therapy on proliferation and apoptosis of cells 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 partialthickness to full-thickness (early stage of formation of HS) were set as pressure treatment group (PT).Another 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 treatment 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 determined with immunohistochemical staining.The apoptosis status was detected with situ end labeling technique.The mRNA expressions of P57kip2 and Cyclin E were determined with real-time fluorescence quantification 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 layer,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 PTM 3,6,12,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 respectively 3.186,2.559,2.880,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 respectively 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 or P <0.01).The mRNA expression of P57kip2 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.