角质形成细胞与皮肤创面愈合瘢痕形成

创伤的愈合是一个复杂的连续的生物学过程，创伤的愈合和组织的重塑有赖于上皮再生、基底膜重建和表皮屏障功能的恢复。随着近年来在细胞生物学、生物化学和分子生物学领域对皮肤创面愈合的研究不断深入，人们对角质形成细胞(KC)在皮肤炎症、创面愈合、瘢痕形成和组织重塑方面起了关键的调节作用这一观点已形成共识。     

培养的正常和瘢痕角质形成细胞上清液对瘢痕成纤维细胞增殖和胶原合成的影响

目的 研究培养的正常角质形成细胞、瘢痕角质形成的细胞的上清液对增生性瘢痕成纤维细胞生物活性和胶原合成的影响。方法 采用MTT、^3H-脯氨酸掺入法、Ⅲ型前胶原放免试剂盒测定不同来源、不同浓茺培养的角度形成细胞上清液，对增生性瘢痕成纤细胞增殖和胶原合成的影响。结果 正常角质形成细胞上清液，可抑制瘢痕成纤维细胞增殖，对细胞内胶原合成有一定的促进作用，但却抑制细胞内胶原向细胞外分泌。瘢痕角质形成细胞上清液，对增生性瘢痕成纤维细胞增殖的抑制作用不明显，甚至还有促进的趋势，对细胞内外胶原合成、分泌皆有明显的促进作用。结论 正常角质形成细胞与瘢痕角质形成细胞分泌的物质对瘢痕成纤维细胞具有不同作用。     

角质形成细胞在色素增加性疾病中的作用研究进展

色素增加性疾病是一类临床上常见的碍容性皮肤病。色素可以分成两大类：一类是内在色素,如黑色素、胆色素等;另一类是外在色素,如食物中的胡萝卜素、药物和重金属。其中尤以黑素细胞合成的黑素过多或分布不均而导致的各类色斑最为常见,并且随着人们生活水平的提高越来越受到广泛的关注。     

角质形成细胞源TGF-β1对成纤维细胞的作用

目的研究正常角质形成细胞分泌的TGF-β1对正常成纤维细胞生物学行为的影响。方法采用免疫组化方法检测角质形成细胞分泌TGF-β1，以不同浓度TGF-β1抗体阻断角质形成细胞条件培养液中的TGF-β1，观察阻断前后角质形成细胞条件培养液对正常成纤维细胞增殖，胶原分泌的影响。结果细胞玻片可见大量染色阳性角质形成细胞，经TGF-β1抗体阻断后的角质形成细胞条件培养液，对成纤维细胞的促增殖作用明显减弱，胶原分泌减少。结论正常角质形成细胞分泌大量TGF-β1，可促进成纤维细胞增殖，促进胶原分泌。     

角质形成细胞源TGF-β_1对成纤维细胞的作用

目的研究正常角质形成细胞分泌的TGF-β1对正常成纤维细胞生物学行为的影响。方法采用免疫组化方法检测角质形成细胞分泌TGF-β1,以不同浓度TGF-β1抗体阻断角质形成细胞条件培养液中的TGF-β1,观察阻断前后角质形成细胞条件培养液对正常成纤维细胞增殖,胶原分泌的影响。结果细胞玻片可见大量染色阳性角质形成细胞,经TGF-β1抗体阻断后的角质形成细胞条件培养液,对成纤维细胞的促增殖作用明显减弱,胶原分泌减少。结论正常角质形成细胞分泌大量TGF-β1,可促进成纤维细胞增殖,促进胶原分泌。     

角质形成细胞条件培养液对成纤维细胞增殖与胶原分泌影响的研究

目的 探讨正常的角质形成细胞对成纤维细胞生物学行为的影响。方法 组织块法培养成纤维细胞，分别加入12．5％、25％与50％浓度的角质形成细胞条件培养液为实验组，加入不含血清DMEM为对照组，采用MTT、羟脯氨酸比色法测定成纤维细胞增殖、胶原合成；以流式细胞仪测定50％浓度角质形成细胞条件培养液组及对照组成纤维细胞生长周期。结果细胞增殖测定，各实验组吸光度（A）值与对照组比较，差异均有统计学意义（P〈0．01）；随浓度增高，A值增加，25％及50％浓度组与12．5％浓度组比较，差异有统计学意义（P〈0．01）；25％及50％浓度组间比较，差异无统计学意义（P〉0．01）。胶原合成测定中，各实验组A值与对照组比较，差异无统计学意义（P〉0．01）；各实验组组间比较，差异无统计学意义（P〉0．01）。细胞周期测定见，50％浓度组可明显促进成纤维细胞通过G1／S及S／G1限制点，S期及G1／M期细胞与对照组相比明显增多，G0／G1期细胞与对照组相比明显减少，差异均有统计学意义（P〈0．01）。结论 正常角质形成细胞的上清液可促进成纤维细胞的增殖，但对其胶原分泌影响不明显。     

角质形成细胞源IL-1α对成纤维细胞增殖及胶原分泌的影响

目的：研究角质形成细胞分泌的IL-1α对成纤维细胞生物学行为的影响。方法：组织块法培养成纤维细胞，消化法培养角质形成细胞，采用免疫组化方法检测角质形成细胞分泌的IL-1α；成纤维细胞中加入含不同浓度IL-1α抗体（0．04μg／ml，0．2μg／ml，1μg／ml）的角质形成细胞条件培养液为实验组，含DMEM的条件培养液为对照组，采用Cell counting kit-8、放免法测定成纤维细胞增殖、胶原合成。结果：细胞爬片可见大量染色阳性角质形成细胞，细胞增殖测定，各实验组吸光度（A）值与对照组比较，差异均有统计学意义（P（0．01）；随抗体浓度增高，A值减小，0．2μg／ml及1μg／ml浓度组与0．04μg／ml浓度组比较，差异有统计学意义（P〈0．01）；胶原分泌浓度测定，各实验组与对照组比较，差异均有统计学意义（P〈0．01）：随抗体浓度及胶原浓度增高，0．2μg／ml及1μg／ml浓度组与0．04μg／ml浓度组比较，差异有统计学意义（P（0．01）。结论：正常角质形成细胞分泌大量IL-1α，可促进成纤维细胞增殖，抑制胶原分泌。     

人瘢痕角质形成细胞原代培养中胰酶配方及浓度的探讨

目的:研究不同配方及浓度的胰蛋白酶对人瘢痕角质形成细胞(Ker at i nocyt e,K)生物活性影响。探索一种更适于瘢痕角质形成细胞原代培养消化的方法。方法:温消化法分离瘢痕组织表皮、真皮后,分别采用0.1%胰蛋白酶和0.05%胰蛋白酶-0.025%EDTA对表皮片进行消化,培养角质形成细胞,用台盼蓝染色法和24h细胞贴壁率观察K存活率及细胞活性。结果:两种配方胰酶消化K,细胞存活率均达80%以上,结果无统计学差异(P>0.05)。与单独使用胰蛋白酶相比,经胰蛋白酶-EDTA组消化后的细胞贴壁率增加,结果有统计学差异(P<0.05)。结论:胰蛋白酶-EDTA能较温和地消化角质形成细胞,较大程度地保留细胞活性,与胰蛋白酶消化法相比,此方法更适合K的消化及培养。     

角质形成细胞在脱细胞异种真皮上培养的实验研究

目的 在脱细胞异种(猪)真皮上培养角质形成细胞探讨体外复合皮的构建。方法 取出生24h内的SD大鼠全厚皮肤，采用低温酶消化法和密度梯度离心法分离获得纯角质形成细胞；以不用任何滋养层的角质形成细胞培养作为空白对照组，脱细胞异种真皮作为支架的角质形成细胞培养为实验组，原代培养后行气——液面培养。形态学，常规组织学HE染色观察，免疫组化染色(SABC法)检测复合皮肤中的Pancyrtokeratin和层粘连蛋白(Laminin)。结果 HE染色显示有4层以上的角质形成细胞和基底膜层形成，并有轻度角质化；免疫组化染色显示：Pancytokeratin( )，提示在脱细胞猪真皮上生长的为角质形成细胞；Laminin( )，提示培养的角质形成细胞产生了新的基底膜。结论 体外培养的角质形成细胞能在脱细胞异种真皮上良好生长、存活，并有基底膜形成，在体外成功构建了具有表皮和真皮的复合皮，可以作为一种新的组织工程化皮肤。     

Pyelonephritic scar formation

Pyelonephritic scars almost never develop after urinary tract infections alone, but require in addition certain risk factors. The most important risk factors are: vesicoureteral reflux, intrarenal reflux, obstructive uropathy, and nephrolithiasis. Most of the pyelonephritic scars develop in early childhood, where we find the combination of vesicoureteral reflux, intrarenal reflux, and urinary tract infections. Urinary tract infections alone almost never result in pyelonephritic scars. After the age of 3 years the risk to develop pyelonephritic scars is not more than 10% in those with the combination of urinary tract infections and vesicoureteral reflux. In this age group the risk to develop pyelonephritic scars is not altered by antireflux operation.     

Dynamic changes of autophagy during hypertrophic scar formation and the role of autophagy intervention

BackgroundThe role of autophagy in the formation of hypertrophic scars (HS) remains unclear. This study aimed to explore the role and potential mechanism of autophagy during the development of HS.MethodsRNA and protein expression levels of Beclin-1, p62, and LC3II in normal skin tissues and HS specimens from different patients were examined. Autophagy inducers and inhibitors were used to cure established HS in rabbit ears, and the expression of Beclin-1, p62, and LC3II at the RNA and protein level was determined. Lastly, the effects of autophagy inducers and inhibitors on HS development were analyzed.ResultsCompared to normal skin tissues, the expression of LC3Ⅱ and Beclin-1 was higher (P<0.05), while that of p62 was lower (P<0.05) in HS tissues. In addition, the LC3II/LC3I ratio was increased during HS formation, and the altered expression of the three proteins stabilized after one year. Administration of autophagy inducers enhanced the formation of HS as well as the expression levels of LC3II and Beclin-1 but decreased p62 expression. Meanwhile, administration of autophagy inhibitors increased the expression of LC3II, Beclin-1, and p62, along with reduced HS formation.ConclusionAutophagic activity increased during HS initiation and subsequent stabilization. In addition, autophagy inhibitors were able to inhibit HS formation by suppressing autophagy, whereas autophagy inducers promoted scar hyperplasia by enhancing autophagy.     

Prevention and treatment of linear scar formation in the scalp: Basic principles of the mechanism of scar formation

Linear scar formation in the scalp after suturing an incision has been considered unavoidable. It was not known why scars formed even if the hair bulb was left intact. The authors developed a subcutaneous tissue-shaving method for radical treatment of bromidrosis and studied the process of hair regeneration by using thick-tissue specimens. They suggest that stem cells (lower) are located not only in the lower end of the telogen hair follicles but also in the sebaceous isthmus at the secretory opening of the sebaceous gland (upper stem cells). They found that linear scars can be prevented and existing linear scars can be surgically treated by using a relaxed suture on a scalp incision to avoid excessive pressure on the upper stem cells.     

他克莫司抑制兔耳瘢痕增生的作用及其机制研究

目的：他克莫司是临床广泛应用的一种药物,其对增生性瘢痕是否产生作用并无相关报道,为此提出并证实了他克莫司可以抑制兔耳瘢痕增生。方法：建立兔耳增生性瘢痕模型,选10只新西兰大耳白兔双耳腹侧用打孔器制作直径1cm圆形创面,伤后14天创面上皮化后给药,每只兔左耳为空白对照组涂等剂量凡士林软膏,右耳为他克莫司治疗组。分别在伤后14天、21天2、8天3、5天和49天采集标本,行HE染色,观察形态学差异;Real-t i me PCR检测纤维化相关因子TGF-β1、TGF-β2、Col l agen-α1等的表达。结果：HE染色可见他克莫司组成纤维细胞数量及胶原纤维较对照组明显减少,PCR结果可见TGF-β1、TGF-β2及Col l agen-α1表达较对照组在各时间点均减少。结论：实验组较对照组瘢痕明显减轻,证明他克莫司显著抑制兔耳瘢痕增生,可作为临床上治疗及预防瘢痕增生的全新疗法。     

尿道瘢痕形成的多因素分析

尿道手术后尿道瘢痕的形成是常见的并发症，常常影响尿道患者的术后康复，一直是泌尿外科医生面临的十分棘手的问题。由于其病因的复杂性，导致治疗效果往往不佳。本文通过对尿道瘢痕相关文献的分析，了解影响尿道瘢痕形成的一些因素，从而为尿道瘢痕的临床预防和治疗奠定理论依据。     

Prevention of postlaminectomy scar formation

An animal experimental study was performed to investigate prevention of scar formation under lumbar laminectomy by using new biodegradable interposing materials-- polylactic acid (PLA) foam and membrane. The experimental animals consisted of 32 dogs, 16 control and 16 experimental. The experimental surgery consisted of L5 or L6 complete laminectomy and covering of the laminectomy defect with the experimental materials. The same procedure but without the covering of the laminectomy defect was performed on the control group animals. Animals were sacrificed at varying intervals (2-52 weeks) and the lumbar spines were evaluated with histologic preparations. The PLA membrane is found to be a promising material for prevention of scar tissue extension and adhesion after laminectomy but has a problem of marginal fitting. PLA foam is found to behave as a scaffold for scar tissue extension and adhesion onto the nerve. Other foamy materials such as gelatin foam or avitane are probably behaving similarly, causing scar tissue extension and adhesion. The new materials were found to be completely biocompatible and slowly biodegradable. A combined use of posteriorly convexed stiff PLA membrane and marginal gap filler with PLA foam may provide solutions for both prevention of scar tissue extension and adhesion and prevention of postlaminectomy spinal stenosis.