| Pathologic scar, including hypertrophic scar (HS) and keloids, is a kind of particular fibro-metabolic disease of derma in the human being. It results from wound, infection, operation and burns, etc, and it's mechanism of formation is very complicated. Hypertrophic scars and keloids are characterized by excessive proliferation of fibroblasts and extracellular matrix (ECM), especially accumulation of collagen. In clinic, both present part-proliferation, pruritus, function hinder and impact on appearance, and the main difference between them are that keloids are characterized by invading peripheral normal tissue and it's tumor-like growth and easily recrudescing after resection etc. The therapy of keloids is a medical sticky difficult problem for surgery, especially for plastic surgery in the world. So to study the mechanism of formation in keloids is still a groping focus in the field of plastic surgery at present. It is well known that the mechanism of formation in keloids is very complicated and related with many cellular factors. Those factors regulate the transform, proliferation, metabolism and apoptosis of fibroblasts. With the rapid development of cell biology and molecular biology, the study of regulating mechanism of wound repair at the level of gene promote the re-understanding of the mechanism of formation in keloids. In 1995, Desmouliere et al put forward that apoptosis may be the one of reason for pathologic scar, and then a lot of researches have been done. Now many scholars have advanced that pathologic scar results from the lack of apoptosis and the block of apoptotic signaling. Once apoptosis active factor is combined with its receptor, the program of apoptosis will be startedup and the death signal will be transferred level by level. In the end, Capsize-3 will be activated and act on the target substance and lead fibroblasts to death.Fas and TNFR1, promotors of apoptosis program, are located in the membrane of fibroblasts.When they are combined with their relevant antibody, the apoptotic path of death receptor will beactivated respectively. Then DISC(death inducing signaling complex) come into being, andfurther activate procaspase-3 which can act on the target substance and make DAN broken, andthe cell dead. In the meanwhile, the path of apoptosis is regulated by many factors in which Bcl-2is more important. Bcl-2, the expressive product of Bcl-2 gene which is recognized as longevousgene, performs a very important role with negative regulation in the path of apoptosis. Bcl-2 canprevent the activating and conduction of apoptosis signaling in many different ways. It isobvious that Fas, TNFR1, Bcl-2 and Caspase-3 act different functions, as follows: start-up,transmit, regulation and taking effect respectively. Therefore a test has been designed to study theexpression and significance of apoptosis-related Fas, Bcl-2 , TNFRi and Caspase-3 in fibroblastsderived from pathologic scar by using immunnohistochemistry method. 40 samples were detectedand the aim is to investigate the relationship between the expression of these proteins and theformation of pathologic scar. It will provide scientific theory for clinical therapy and a new way ofpreventing and treating pathologic scar.Materials and methods:40 samples, including 15 keloids tissues, 15 hypertrophic scars and 10 normal skins, were collected from 40 patients who were undergone plastic surgery in the First Affiliated Hospital of Zhengzhou University. Among the samples, the Hypertrophic tissues were cut from face(3 cases), neck(2 cases), chest(4 cases), upper limbers (3 cases)and legs(3 cases) ; keloids tissues were cut from earlobe(9 cases), chest(3 cases) and back(3 cases) ; the normal skins were cut from abdomen and limbs. The other clinical information: 1. HS Duration: 1-3 years. The patients included 9 males and 6 females and their age ranged from 3.5 to 43 years old. Hypertrophic scar remains with the boundaries of the original wound. 2. Keloids Duration: 3-5 years. The patients included 2 males and 13 female... |
PDF Full Text Request