TGF-β change in blister fluid of hypertrophic scar and its significance

Objective To investigate of the tissue TGF-β changes at early stage of hypertrophic scar formation and the value of scar blisters in hypertrophic scar.Methods The TGF-β1 content in the blister fluid and the blood were quantified with ELISA,patients(n=15)with hypertrophy scar after depth burn were included,three time point(each n=5)on early　stage(<3 months)of hypertrophy scar formation were monitored.and normal skin blister fluid and the blood(n=5)was used as control.Results The serum TGF-β1 in the both hypertrophic scar patients and normal skin group was not elevated(P>0.01),the TGF-β1 in the blister of normal skin was also not elevated(P>0.01),but TGF-β1 level in the scarblisters hypertrophic scar was elevated significantly[<60 d(158.5±69.8)pg/L,60-90 d,(181.1±40.1)pg/L,>90 d,(534.4±125.9)pg/L,P<0.01] and higher than the normal skin blister and the blood(P<15.6 pg/L.P<0.01),the increased TGF-β1 1evel in the hypertrophic scar blisters were persisted for at least three months.the TGF-β1 level of scar blister on the 3th month of hypertrophic scar formation reached a peak [(534.4±125.9)pg/L,P<0.01].Conclusions The data in this study indicates that TGF-β production at the early stage of hypertrophic scar formation is increased and may play an important role in scar formation;scar blisters is a valuable approach in hypertrophic scar study.     

TGF-β change in blister fluid of hypertrophic scar and its significance

Objective To investigate of the tissue TGF-β changes at early stage of hypertrophic scar formation and the value of scar blisters in hypertrophic scar.Methods The TGF-β1 content in the blister fluid and the blood were quantified with ELISA,patients(n=15)with hypertrophy scar after depth burn were included,three time point(each n=5)on early　stage(<3 months)of hypertrophy scar formation were monitored.and normal skin blister fluid and the blood(n=5)was used as control.Results The serum TGF-β1 in the both hypertrophic scar patients and normal skin group was not elevated(P>0.01),the TGF-β1 in the blister of normal skin was also not elevated(P>0.01),but TGF-β1 level in the scarblisters hypertrophic scar was elevated significantly[<60 d(158.5±69.8)pg/L,60-90 d,(181.1±40.1)pg/L,>90 d,(534.4±125.9)pg/L,P<0.01] and higher than the normal skin blister and the blood(P<15.6 pg/L.P<0.01),the increased TGF-β1 1evel in the hypertrophic scar blisters were persisted for at least three months.the TGF-β1 level of scar blister on the 3th month of hypertrophic scar formation reached a peak [(534.4±125.9)pg/L,P<0.01].Conclusions The data in this study indicates that TGF-β production at the early stage of hypertrophic scar formation is increased and may play an important role in scar formation;scar blisters is a valuable approach in hypertrophic scar study.     

多沙唑嗪对兔膀胱出口部分梗阻致膀胱顺应性减低的影响

目的 探讨多沙唑嗪对兔膀胱出口部分梗阻后膀胱顺应性改变的影响.方法 成年雄性新西兰兔40只随机分为4组,每组10只,A组为假手术对照组,B组为膀胱出口部分梗阻组,C组为膀胱出口部分梗阻后口服多沙唑嗪组,D组为假手术后给予多沙唑嗪组.各组于14周行尿动力学检测,检测完成后处死并留取膀胱标本,行膀胱称重.结果 4组膀胱标本质量分别为(3.2±0.9)、(14.1±2.3)、(5.0±2.0)、(2.9±0.5)g;B、C组均高于A、D组,B组高于C组,差异均有统计学意义(P＜0.01);A、D组间比较差异无统计学意义(P＞0.05).4组逼尿肌漏尿点压分别为(10.2±2.5)、(18.8±6.1)、(13.5±4.7)、(11.6±3.6)cm H2O(1 cm H2O=0.098 kPa),B组高于A、D组,差异有统计学意义(P＜0.01),且高于C组,差异有统计学意义(P＜0.05);A、C、D组间差异无统计学意义(P＞0.05).膀胱顺应性分别为(2.86±0.56)、(1.22±0.39)、(4.25±2.19)、(2.90±0.53)ml/cm H2O,B组与A、D组相比明显下降,差异有统计学意义(P＜0.01);C组高于A、D组,差异有统计学意义(P＜0.05);A、D组间差异无统计学意义(P＞0.05).结论膀胱出口部分梗阻后早期应用多沙唑嗪治疗能够延迟梗阻对膀胱顺应性的损害,保护膀胱储尿功能.

Abstract：

Objective To explore the effect of doxazosin on rabbit bladder compliance after partial bladder outlet obstruction. Methods A total of 40 male New Zealand white rabbits were randomized into 4 groups, with 10 rabbits in each group. Partial bladder outlet obstruction was established in groups B and C, while groups A and D underwent the same operation but without partial bladder outlet obstruction. On the day after the operation, groups C and D received oral administration of doxazosin. After 14 weeks, urodynamic examinations were carried out in all groups, and the bladder was weighted after cystectomy. Results Bladder weight was (3.2±0.9) g in group A, (14.1±2.3) g in group B, (5.0±2.0) in group C,and (2.9±0.5) g in group D. The bladder weight in groups B and C increased significantly compared to groups A and D (P＜0.01), group B increased significantly over group C (P＜0.01), and there was no significant difference between groups A and D (P＞0.05).The detrusor leak point pressure was (10.2±2.5) cm H2O in group A, (18.8±6.1) cm H2O in group B, (13.5±4.7) cm H2O in group C,and (11.6±3.6) cm H2O in group D. The detrusor leak point pressure in group B was significantly higher than group A, group D (P＜0.01) and group C (P＜0.05). There was no significant difference between group A, group C and group D (P＞0.05). The bladder compliance was (2.86±0.56) ml/cm H2O in group A, (1.22±0.39) ml/cm H2O in group B, (4.25±2.19) ml/cm H2O in group C,and (2.90±0.53) ml/cm H2O in group D. The bladder compliance was significantly decreased in group B compared to groups A and D (P＜0.01). Bladder compliance in group C was significantly higher than in groups A and D (P＜0.05), and there was no significant difference between group A and group D (P＞0.05). Conclusion Early use of doxazosin can delay the occurrence of lower bladder compliance after partial bladder outlet obstruction, thus protecting the storage function of bladder.     

心脏不停跳修补室缺后肌钙蛋白T分泌变化

目的 观察心脏不停跳修补室缺后肌钙蛋白T(cTnT)分泌变化.方法 共施行单纯室间隔缺损(VSD)合并轻、中度肺动脉高压患者202例.VSD(0.7 ±0.2)cm;膜部185例,干下型15例,肌部2例.心胸比例0.49 ±0.18.随机分为3组:A组(晶体组)86例;B组(血灌组)51例;C组(不停跳组)65例.术中切取右心耳行电镜观察.术后24 h和72 h抽血监测cTnT.结果 无气栓、死亡、严重低心排、肾功能或呼吸功能衰竭等严重并发症发生.术后1～2 d轻度血红蛋白尿5例.术后1～3 d暂时性房室分离7例.直径＜2 mm残余漏2例.C组2例术中室颤.手术后24 h的cTnT:A组(0.75±0.25)μg/L与B组(0.69 ±0.20)μg/L,P＞0.05,C组(0.55 ±0.18)μg/L与A、B组差异有统计学意义(P＜0.01).术后72 h的cTnT:A组(0.53 ±0.19)μg/L与C组(0.55±0.13)μg/L,P＞0.05,A组与B组(0.43±0.13)μg/L,P＜0.01.电镜发现3组之间,以C组损害略轻,A组相对较重.结论 心脏跳动下修补可明显减少手术时间,由此可以减少由手术对全身造成的创伤,并且方法安全、可行.心脏不停跳修补的cTnT分泌变化反映了心肌保护效果:并不优于血灌组,两者皆优于晶体停跳组.

Abstract：

Objective To estimate the myocardial protective effect of the operation.Methods From January 2004 to June 2009,we implemented ventricular septal defect (VSD) repairs in 202 patients with simple VSD and mild and moderate pulmonary hypertension,including 98 males and 104 females.Theaverage size of VSD was (0.7 ±0.2) cm.There were 185 patients with perimenbranous VSD,15 patients with lower trunk VSD,and 2 patients with muscular VSD.The average cardiothoracic ratio (CTR) was 0.49 ±0.18.202 patients were randomly divided into 3 groups:group A (crystalloid group) with 86 cases;group B (hemoperfusion group) with 51 cases;group C (beating heart group) with 65 cases.During the operation,right atrial appendage muscle was cut off and observed under the electron microscopy.The blood cardiac Troponin T (cTnT) was examined 24 and 72 h postoperation.Results There was no air embolism,death,severe low cardiac output,renal or respiratory failure or other serious complications.One to2 days after surgery,5 cases had mild hemoglobinuria.One-3 days after surgery,7 cases had a temporary atrioventricular separation.There were 2 cases of residual leakage with the diameters both below 2 mm.Two cases in group C suffered from ventricular fibrillation during operation.At 24th h after surgery,there was no significant difference in cTnT ( P ＞ 0.05 ) between group A (0.75 ± 0.25 ) μg/L and group B (0.69 ±0.20) μg/L,and there was statistically great significant difference between group C (0.55 ±0.18) μg/L and groups A or B (P＜0.01).At tge 72nd h after surgery,there was no significant difference in the cTnT level ( P ＞ 0.05 ) between group A (0.53 ± 0.19 ) μg/L and group C ( 0.55 ± 0.13 )μg/L,but there was statistically great significant difference between group A and group B (0.43 ±0.13)μg/L (P ＜0.01 ).The damage in group C was milder,and that in group A was severer.Conclusion Beating heart surgery can significantly reduce the operative duration of VSD repair,thereby it can limit the surgical trauma on the body.Moreover,the method is conservative and practical.In terms of changes of cTnT secretion or myocardial protective effect for repair of VSD,the beating heart surgery was not superior to the hemoperfusion group while both of the groups were superior to the crystalloid group.     

L-精氨酸和氨基胍在大鼠肺移植缺血再灌注损伤中的作用

目的 观察L-精氨酸(L-Arg)和氨基胍对大鼠肺移植后缺血再灌注的保护作用.方法 建立大鼠左单肺移植模型,术后随机分为A组(对照组,腹腔注射生理盐水),B组(腹腔注射L-Arg)、C组(腹腔注射氨基胍)和D组(腹腔注射L-Arg和氨基胍),每组6只.移植肺再灌注2 h后,检测肺组织髓过氧化物酶(MPO)、丙二醛(MDA)含量、超氧化物歧化酶(SOD)活力、内皮型一氧化氮合酶(eNOS)和诱导型一氧化氮合酶(iNOS)活性并测定移植肺干湿重比(W/D)及静脉血中一氧化氮(NO)含量,观察移植肺的病理学形态.结果 再灌注2 h后,B组移植肺的W/D(5.10±0.21)、MPO(1.74±0.26)U/g和MDA(20.87±2.90)μmol/g均低于A组W/D(5.74 ±0.14)、MPO(2.36±0.32)U/g和MDA(31.33 ±3.46)μmol/g;SOD活性(424.29±27.86)U/mgprot、NO含量(175.12 ±17.40)μmol/L、iNOS活性(3.62 ±0.26)U/mgprot和eNOS活性(5.36±0.28)U/mgprot均较A组SOD活性(268.01±26.06)U/mgpro、NO含量(98.29±6.95)μmol/L、iNOS活性(2.53 ±0.22)U/mgprot和eNOS活性(3.57 ±0.40)U/mgprot高(P＜0.05).C组的NO含量(84.13±5.18)μmol/L、iNOS活性(1.81 ±0.09)U/mgprot均较A组低(P＜0.05).D组的W/D(4.79 ±0.19)、MPO(1.24±0.13)U/g、MDA(14.60±4.14)μmol/g、iNOS活性(1.99±0.17)U/mgprot低于A组,SOD活性(493.75±24.95)、NO含量(149.61±10.70)μmol/L、eNOS活性(5.50±0.27)U/mgprot高于A组(P＜0.05).与B组比较,D组的W/D、MPO、MDA、NO含量、iNOS活性降低,SOD升高(P＜0.05).病理形态学检查显示D组炎细胞浸润及渗出最轻,B组次之,A组和C组最差.结论 移植后再灌注早期应用L-Arg可减轻缺血再灌注损伤,应用氨基胍并不能减轻移植肺的损伤,但联合应用L-Arg和氨基胍优于单纯应用L-Arg.

Abstract：

Objective To investigate the effects of L-arginine (L-Arg) and aminoguanidine on ischemia-reperfusion injury following rat lung transplantation. Methods The models of rats lung transplantation were established and 4 groups ( n = 6 each) were randomly set up: group A ( normal control group)and treated groups B, C and D. In these groups, different medicines (NS, group A; L-Arg, group B;aminoguanidine, group C; L-Arg and aminoguanidine, group D) were intraperitoneally administered to the recipient rats before reperfusion. After reperfusion for 2 h, the lung graft was harvested for measurements of lung wet/dry ratio ( W/D ) , myeloperoxidase ( MPO ) , malondialdehyde ( MDA ) , superoxide dismutase (SOD) , endothelial nitric oxide synthase (eNOS) , inducible nitric oxide synthase (iNOS). The contents of plasma nitric oxide (NO) were determined. The pathological changes in the lung grafts were observed.Results After reperfusion for 2 h, W/D (5. 10 ±0.21), MPO (1.74 ±0.26) U/g, MDA (20.87 ±2. 90) μmol/g in group B were significantly lower [W/D (5. 74 ± 0. 14), MPO (2. 36 ± 0. 32) U/g,MDA (31. 33 ±3.46) μmol/g] (P ＜ 0. 05), and the levels of SOD (424. 29 ± 27. 86) U/mg protein,NO (175. 12 ± 17. 40) μmol/L, iNOS (3. 62 ±0. 26) U/mg protein and eNOS (5. 36 ±0. 28) U/mg protein were significantly higher than in group A [SOD (268.01 ±26.06) U/mg protein, NO (98.29 ±6.95) μmol/L, iNOS (2.53 ±0.22) U/mg protein and eNOS (3. 57 ±0.40) U/mg protein] (P＜0. 05). The contents of NO (84. 13 ±5. 18) μmol/L and iNOS (1. 81 ±0. 09) U/mg protein in group C were significantly lower than in group A (P ＜ 0. 05). W/D (4. 79 ± 0. 19) , MPO (1. 24 ± 0. 13 ) U/g,MDA (14. 60 ±4. 14) μmol/g, iNOS (1. 99 ±0. 17) U/mg protein were significantly lower than in group A (P ＜0. 05) , and SOD (493. 75 ±24. 95) , NO (149. 61 ± 10. 70) μmol/L and eNOS (5. 50 ±0. 27)U/mg protein in group D were significantly higher than in group A (P＜0. 05). W/D, MPO, MDA, NO and iNOS in group D were significantly reduced as compared with group B (P ＜ 0. 05 ) , and SOD was significantly increased in group B ( P ＜ 0. 05 ) . The pathological examination revealed that the inflammatory cell infiltration in group D was the mildest, followed by groups B, A and C. Conclusion The L-Arg could alleviate the lung ischemia-reperfusion injury after transplantation, the combined used of L-Arg and aminoguanidine could obtain better effects than L-Arg used alone. The aminoguanidine used alone could not alleviate ischemia-reperfusion injury after transplantation.     

γ干扰素对小鼠骨骼肌钝挫伤后转化生长因子-β-Smad信号通路表达的影响

目的 观察γ干扰素(IFN-γ)局部注射对小鼠骨骼肌钝挫伤后纤维化以及转化生长因子-β(TGF-β)-Smad信号通路表达的影响.方法 将30只成年雌性C57bl小鼠随机分为正常组(A组)、磷酸盐缓冲液(PBS)注射组(B组)和hIFN-γ注射组(C组),每组10只.B、C组采用50g钢球于30cm高度下砸的方法 造成双侧腓肠肌钝挫伤,分别于伤后1、2、3周局部皮下注射0.1ml PBS或hIFN-γ,A组不行任何处理;4周后取双侧腓肠肌检测.以Masson染色后计算胶原纤维面积评估骨骼肌纤维化程度,Western blot检测TGF-β1、Smad2、Smad3、Smad4、Smad7蛋白表达水平.结果 Masson染色显示B组胶原面积最大为(14074.0±15.2)μm2(P<0.05),C组为(4019.0±13.4)μm2高于A组(1741.0±10.1)μm2(P<0.05);TGF-β1在B、C组表达增高(P<0.05),但两组之间表达差异无统计学意义(P>0.05);3组间Smad4、7的表达差异无统计学意义(P>0.05);Smad2、3及其磷酸化蛋白在B、C组表达升高(P<0.05),其中磷酸化的Smad2、3 在C组较B组表达明显降低(P<0.05).结论 局部注射hIFN-γ,未发现影响TGF-β1的表达,但能够有效降低Smad2、3磷酸化蛋白的表达,可能是其抑制损伤骨骼肌纤维化的作用机制.

Abstract：

Objective To observe the influence of local injection of human interferon γ (hIFN-γ) on the fibrosis and transforming growth factor-β1 (TGF-β1)-Smad signal pathway in the skeletal muscle following acute contusion. Methods Thirty female C57bl mice were randomly divided into 3 groups as A, B and C. The mice in groups B and C were injured by heavy hit of a 50 g ball from 30 cm height to establish gastrocnemius contusion models, and then subcutaneously injected with 0.1 ml PBS and hIFN-γ respectively. No interference was given to group A. All mice were sacrificed 4 weeks later to harvest the gastrocnemius. Fibrosis was estimated by calculating collagen areas on masson staining section. Expression of the proteins as TGF-β1, Smad2, Smad3, Smad4 and Smad7 was detected by Western blotting. Results The collagen area on masson staining section of group B was the greatest as (14 074.0±15.2) μm2, and that in group C was (4019.0±13.4) μm2, greater than that in group A (1741.0±10.1) μm2 (P<0.05). The level of TGF-β1 was increased in both groups B and C, but without statistically significant difference between them (P>0.05). No significant difference was found in Smad4 and Smad7 protein expression among three groups (P>0.05). Total Smad2 and Smad3 were increased in groups B and C but without significant difference (P>0.05). Phosphorylated Smad2/3 level was also increased in both groups B and C, and that was lower in group C (P<0.05). Conclusion Without influence on the expression of TGF-β1, local injection of hIFN-γ could reduce the phosphorylation of Smad2/3 significantly, which probably contributed to the suppression of fibrosis within injured skeletal muscle.     

低温保存不同时间大鼠带瓣管道活性与bax、bcl-2基因表达的关系

目的 观察低温保存不同时间大鼠带瓣血管活性及bax和bcl-2基因的表达,探讨基因检测是否能成为带瓣血管活性指标.方法 Wistar大鼠80只,体质量250～350 g,分为新鲜组A组,-196 ℃液氮冻存3、6、9个月为B、C、D 3组.检测细胞结构、糖代谢及bax、bcl-2基因的变化.结果 大鼠带瓣血管的各组葡萄糖代谢率测定,A组(4.365±0.784)与B(4.383±0.548)、C组(4.446±0.608)、D组(4.090±0.657)差异无统计学意义(P＞0.05);bax基因的表达分别为20%、45%、60%和85%,差异有统计学意义(P＜0.05);bcl-2基因表达分别25%、30%、20%和35%,差异无统计学意义(P＞0.05).结论 经冻存后的大鼠带瓣血管活性良好,提示bax基因可作为检测带瓣血管活性的指标,bcl-2的表达或高表达可能是细胞能耐受冻存打击的原因之一.

Abstract：

Objective To study the expression of bax and bcl-2 genes and activity of valved conduit in rats by cryopreservation for different lengths, and to probe whether genetic detection will become one of the indexes of valved conduit activity. Methods Eighty Wistar rats were divided into four groups: 20cases of fresh blood vessels ( group A ), 20 cases of frozen vessels for 3 months ( group B ), 20 for 6months ( group C), and 20 for 9 months ( group D). The changes in cellular structure, gluoce metabolism and the expression of bax and bcl-2 proteins were observed. Results The glucose metabolism rate of the rate valved conduit in groups A, B, C and D was 4. 365 ± 0. 784, 4. 383 ± 0. 548, 4. 446 ± 0. 608, and 4. 090 ± 0. 657 respectively, with the difference being not significant ( P ＞ 0. 05 ). The positive expression rate of bax protein in groups A, B, C and D was 20%, 45%, 60% and 85% respectively (P＜0. 05).The positive expression rate of bcl-2 in groups A, B, C and D was 25%, 30%, 20% and 35% respectively ( P ＞ 0. 05 ). Conclusion The frozen rat valved vascular showed good activity. bax gene can be regarded as one of the indicators for detecting valved vessel activity. The expression or over-expression of bcl-2gene may be one of the reasons why the cells can tolerate the frozen preservation.     

反义寡核苷酸对TGF-β1诱导的人增生性瘢痕成纤维细胞的影响

目的 观察结缔组织生长因子(CTGF)反义寡核苷酸(ASODN)对转化生长因子β1(TGF-β1)诱导的人增生性瘢痕成纤维细胞(HSF)的影响,探讨CTGF ASODN对人增生性瘢痕的作用.方法 将体外分离、培养的人正常皮肤成纤维细胞(NSF)和HSF分成A(NSF)、B(HSF)、C(HSF+TGF-β1)、D(HSF+TGF-β1+CTGFASODN)四组.经TGF-β1(5.0μg/L)诱导HSF后,将CTGFASODN以脂质体介导的方法转染HSF.用RT-PCR方法检测四组中CTGF mRNA的表达,用MTT比色法和流式细胞仪分别检测转染6、12、24、48、72 h的成纤维细胞的增殖和凋亡情况.结果 CTGF mRNA在NSF中的表达极其微弱;在HSF中,B组的表达量为0.31±0.14,C组的表达量为0.64±0.32,D组的表达量为0.12±0.62.A组与B、C、D组比较,其差异有统计学意义(P<0.05);而D组与B、C组比较,其差异也有统计学意义(P<0.05).结论 CTGF ASODN具有降低HSF中CTGF的表达从而延缓瘢痕纤维化的作用,可能成为治疗瘢痕增生的有效手段.     

氟尿嘧啶植入剂对H22肝癌移植瘤射频消融后残留癌的抑制作用及其机制

目的 探讨氟尿嘧啶植入剂对H22肝癌移植瘤射频消融(RFA)后残留癌的作用及其机制.方法 采用H22肝癌小鼠移植瘤模型,建立RFA后残留癌模型.随机分为5组:不作任何处理(A组);单纯RFA处理(B组);RFA后残留癌内分别植入氟尿嘧啶植入剂2 mg(C组)、4 mg(D组)和6 mg(E组).RFA两周后取残留癌组织,免疫组织化学方法检测增殖细胞核抗原(PCNA)、血管内皮生长因子(VEGF)、微血管密度(MVD)的表达;Western blot法检测PCNA和VEGF的蛋白表达.结果 与A组(2.51±0.30)cm3比较,B组肿瘤体积明显增大(3.10±0.20)cm3,C、D和E组肿瘤体积逐渐减小,分别为(1.51±0.20)、(0.72±0.45)、(0.36±0.22)cm3(P＜0.05).与A组(1.40±0.25)g比较,B组取瘤时瘤重明显增加为(2.51±0.37)g,C、D和E组取瘤时瘤重逐渐减轻,分别为(1.33±0.22)、(0.80±0.21)、(0.01±0.01)g(P＜0.05).B、C、D和E组的抑瘤率分别为-79%、5%、43%和99%.免疫组织化学结果:与A组比较,B组残留癌中VEGF、PCNA和MVD的表达均明显增高,C、D和E组残留癌中VEGF、PCNA和MVD的表达逐渐减少(P＜0.05).Western blot结果,与A组比较,B组残留癌中VEGF和PCNA的蛋白表达均明显增高,C、D和E组残留癌中VEGF和PCNA的蛋白表达逐渐减少(P＜0.05).结论 氟尿嘧啶植入剂对H22肝癌移植瘤RFA后残留癌有明显的抑制作用,并可能通过抑制肿瘤细胞生长和血管生成而抑制残留癌的生长.

Abstract：

Objective To evaluate the effect and mechanism of fluorouracil implants on residual tumor of mouse H22 model following radiofrequency ablation (RFA). Methods The mouse H22 model was established. The tumors were subjected to RFA under the ablation condition of 55 ℃ for 5 min. Fifty-five mouse H22 models were divided into five groups randomly: control group ( group A); RFA group (group B); combined treatments group using RFA and 2 mg fluorouracil implants (group C), 4 mg flu orouracil implants ( group D) and 6 mg fluorouracil implants ( group E). The change of tumor volumes,and tumor weights were detected two weeks after RFA. The microvessel densities (MVD) of the residual tumor were measured by immunohistochemical staining. The expression of vascular endothelial growth factor (VEGF) and proliferating cell nuclear antigen (PCNA) were examined by immunohistochemical staining and Western blotting. Results As compared with group A (2. 51 ± 0. 30) cm3, tumor volumes in group B were statistically increased (3. 10 ±0. 20) cm3, those in group C (1.51 ±0. 20) cm3, group D (0. 72 ± 0. 45) cm3 and group E (0. 36 ± 0. 22) cm3 were gradually decreased ( P ＜ 0. 05 ). As compared with group A ( 1.40 ±0. 25) g, the tumor weights in group B were statistically increased (2.51 ±0. 37) g, but those in group C ( 1.33 ±0. 22 g), group D (0. 80 ±0. 21 ) g and group E (0. 01 ±0. 01 ) g were gradually decreased (P ＜0. 05). The inhibiton rate of tumor growth in groups B, C, D and E was - 79%, 5%,43% and 99% respectively. Immunohistochemical staining indicated that the expression levels of VEGF,PCNA and MVD in group B were significantly higher than those in group A, but those in groups C, D and E were gradually lower than those in group A ( P ＜ 0. 05 ). Western blotting revealed that the protein expression levels of VEGF and PCNA in group B were significantly higher than those in group A, but those of VEGF and PCNA in groups C, D and E were gradually lower than those in group A (P＜0. 05). Conclusion Fluorouracil implants inhibits residual tumor of mouse H22 model following RFA significantly by inhibiting the growth and angiogenesis of residual tumor.     

A型肉毒毒素局部应用对兔耳增生性瘢痕创面愈合和瘢痕增生的影响

Objective To investigate the effect of botulinum toxin type A (Botox A) injection on hypertrophic scar in rabbit ear model. Methods The hypertrophic scar model was established in 16 Japanese rabbits' ears. These wounds were divided into two groups as group T(treated with Botox A, n =48) and group S (not treated, n = 48). The wounds healing times and scar hypertrophy were observed with 8 specimen of normal skin at the rabbit ears as sham group B. HE stain was used to assess the hypertrophic index(HI). The expression of collagen Ⅰ and Ⅲ was tested by western-blot. The cell cycle of fibroblasts was studied by flow cytometry. Results The [] was significantly lower in group T than in group S(P < 0.01). The expression of collagen Ⅰ and Ⅲ, as well as the ratio of Ⅰ to Ⅲ, was markedly stronger in group S than in group T(P < 0.01). Compared with group T, more fibroblasts were in G2-M in gToup S and fewer in G0-G1 (P <0.05). Conclusions Local injection of Botox A can inhibite the formation of hypertrophic scar and the activity of fibroblasts in rabbit ear model. It can significantly decrease the expression of collagen Ⅰ and Ⅲ in hypertrophic scar, as well as the ratio of collagen Ⅰ to Ⅲ. It serves as the basis for the treatment of hypertrophic scar with Botox A.     

A型肉毒毒素局部应用对兔耳增生性瘢痕创面愈合和瘢痕增生的影响

Objective To investigate the effect of botulinum toxin type A (Botox A) injection on hypertrophic scar in rabbit ear model. Methods The hypertrophic scar model was established in 16 Japanese rabbits' ears. These wounds were divided into two groups as group T(treated with Botox A, n =48) and group S (not treated, n = 48). The wounds healing times and scar hypertrophy were observed with 8 specimen of normal skin at the rabbit ears as sham group B. HE stain was used to assess the hypertrophic index(HI). The expression of collagen Ⅰ and Ⅲ was tested by western-blot. The cell cycle of fibroblasts was studied by flow cytometry. Results The [] was significantly lower in group T than in group S(P < 0.01). The expression of collagen Ⅰ and Ⅲ, as well as the ratio of Ⅰ to Ⅲ, was markedly stronger in group S than in group T(P < 0.01). Compared with group T, more fibroblasts were in G2-M in gToup S and fewer in G0-G1 (P <0.05). Conclusions Local injection of Botox A can inhibite the formation of hypertrophic scar and the activity of fibroblasts in rabbit ear model. It can significantly decrease the expression of collagen Ⅰ and Ⅲ in hypertrophic scar, as well as the ratio of collagen Ⅰ to Ⅲ. It serves as the basis for the treatment of hypertrophic scar with Botox A.     

A型肉毒毒素局部应用对兔耳增生性瘢痕创面愈合和瘢痕增生的影响

Objective To investigate the effect of botulinum toxin type A (Botox A) injection on hypertrophic scar in rabbit ear model. Methods The hypertrophic scar model was established in 16 Japanese rabbits' ears. These wounds were divided into two groups as group T(treated with Botox A, n =48) and group S (not treated, n = 48). The wounds healing times and scar hypertrophy were observed with 8 specimen of normal skin at the rabbit ears as sham group B. HE stain was used to assess the hypertrophic index(HI). The expression of collagen Ⅰ and Ⅲ was tested by western-blot. The cell cycle of fibroblasts was studied by flow cytometry. Results The [] was significantly lower in group T than in group S(P < 0.01). The expression of collagen Ⅰ and Ⅲ, as well as the ratio of Ⅰ to Ⅲ, was markedly stronger in group S than in group T(P < 0.01). Compared with group T, more fibroblasts were in G2-M in gToup S and fewer in G0-G1 (P <0.05). Conclusions Local injection of Botox A can inhibite the formation of hypertrophic scar and the activity of fibroblasts in rabbit ear model. It can significantly decrease the expression of collagen Ⅰ and Ⅲ in hypertrophic scar, as well as the ratio of collagen Ⅰ to Ⅲ. It serves as the basis for the treatment of hypertrophic scar with Botox A.     

肉毒毒素A对大鼠皮肤及创面组织中SP、CGRP、TGF-β1和α-SMA的影响

Objective To investigate the effect of botulinum toxin type A (Botox A) injection on hypertrophic scar in rabbit ear model. Methods The hypertrophic scar model was established in 16 Japanese rabbits' ears. These wounds were divided into two groups as group T(treated with Botox A, n =48) and group S (not treated, n = 48). The wounds healing times and scar hypertrophy were observed with 8 specimen of normal skin at the rabbit ears as sham group B. HE stain was used to assess the hypertrophic index(HI). The expression of collagen Ⅰ and Ⅲ was tested by western-blot. The cell cycle of fibroblasts was studied by flow cytometry. Results The [] was significantly lower in group T than in group S(P < 0.01). The expression of collagen Ⅰ and Ⅲ, as well as the ratio of Ⅰ to Ⅲ, was markedly stronger in group S than in group T(P < 0.01). Compared with group T, more fibroblasts were in G2-M in gToup S and fewer in G0-G1 (P <0.05). Conclusions Local injection of Botox A can inhibite the formation of hypertrophic scar and the activity of fibroblasts in rabbit ear model. It can significantly decrease the expression of collagen Ⅰ and Ⅲ in hypertrophic scar, as well as the ratio of collagen Ⅰ to Ⅲ. It serves as the basis for the treatment of hypertrophic scar with Botox A.     

A型肉毒毒素局部应用对兔耳增生性瘢痕创面愈合和瘢痕增生的影响

Objective To investigate the effect of botulinum toxin type A (Botox A) injection on hypertrophic scar in rabbit ear model. Methods The hypertrophic scar model was established in 16 Japanese rabbits' ears. These wounds were divided into two groups as group T(treated with Botox A, n =48) and group S (not treated, n = 48). The wounds healing times and scar hypertrophy were observed with 8 specimen of normal skin at the rabbit ears as sham group B. HE stain was used to assess the hypertrophic index(HI). The expression of collagen Ⅰ and Ⅲ was tested by western-blot. The cell cycle of fibroblasts was studied by flow cytometry. Results The [] was significantly lower in group T than in group S(P < 0.01). The expression of collagen Ⅰ and Ⅲ, as well as the ratio of Ⅰ to Ⅲ, was markedly stronger in group S than in group T(P < 0.01). Compared with group T, more fibroblasts were in G2-M in gToup S and fewer in G0-G1 (P <0.05). Conclusions Local injection of Botox A can inhibite the formation of hypertrophic scar and the activity of fibroblasts in rabbit ear model. It can significantly decrease the expression of collagen Ⅰ and Ⅲ in hypertrophic scar, as well as the ratio of collagen Ⅰ to Ⅲ. It serves as the basis for the treatment of hypertrophic scar with Botox A.     

A型肉毒毒素局部应用对兔耳增生性瘢痕创面愈合和瘢痕增生的影响

Objective To investigate the effect of botulinum toxin type A (Botox A) injection on hypertrophic scar in rabbit ear model. Methods The hypertrophic scar model was established in 16 Japanese rabbits' ears. These wounds were divided into two groups as group T(treated with Botox A, n =48) and group S (not treated, n = 48). The wounds healing times and scar hypertrophy were observed with 8 specimen of normal skin at the rabbit ears as sham group B. HE stain was used to assess the hypertrophic index(HI). The expression of collagen Ⅰ and Ⅲ was tested by western-blot. The cell cycle of fibroblasts was studied by flow cytometry. Results The [] was significantly lower in group T than in group S(P < 0.01). The expression of collagen Ⅰ and Ⅲ, as well as the ratio of Ⅰ to Ⅲ, was markedly stronger in group S than in group T(P < 0.01). Compared with group T, more fibroblasts were in G2-M in gToup S and fewer in G0-G1 (P <0.05). Conclusions Local injection of Botox A can inhibite the formation of hypertrophic scar and the activity of fibroblasts in rabbit ear model. It can significantly decrease the expression of collagen Ⅰ and Ⅲ in hypertrophic scar, as well as the ratio of collagen Ⅰ to Ⅲ. It serves as the basis for the treatment of hypertrophic scar with Botox A.     

A型肉毒毒素局部应用对兔耳增生性瘢痕创面愈合和瘢痕增生的影响

Objective To investigate the effect of botulinum toxin type A (Botox A) injection on hypertrophic scar in rabbit ear model. Methods The hypertrophic scar model was established in 16 Japanese rabbits' ears. These wounds were divided into two groups as group T(treated with Botox A, n =48) and group S (not treated, n = 48). The wounds healing times and scar hypertrophy were observed with 8 specimen of normal skin at the rabbit ears as sham group B. HE stain was used to assess the hypertrophic index(HI). The expression of collagen Ⅰ and Ⅲ was tested by western-blot. The cell cycle of fibroblasts was studied by flow cytometry. Results The [] was significantly lower in group T than in group S(P < 0.01). The expression of collagen Ⅰ and Ⅲ, as well as the ratio of Ⅰ to Ⅲ, was markedly stronger in group S than in group T(P < 0.01). Compared with group T, more fibroblasts were in G2-M in gToup S and fewer in G0-G1 (P <0.05). Conclusions Local injection of Botox A can inhibite the formation of hypertrophic scar and the activity of fibroblasts in rabbit ear model. It can significantly decrease the expression of collagen Ⅰ and Ⅲ in hypertrophic scar, as well as the ratio of collagen Ⅰ to Ⅲ. It serves as the basis for the treatment of hypertrophic scar with Botox A.