| BackgroundChronic wounds (commonly known as ulcers) are caused by a variety of wounds and disease, can not through the normal timely and orderly repair process to complete anatomical and functional healing. In clinical, it refers to the wounds that has no healing or healing tendency by the treatment more than a month, including traumatic ulcers, lower extremity venous ulcers, pressure ulcers and diabetic ulcers. It occurs in the surface, has a complex etiology, duration, difficulty in treatment, more complications, vulnerability to relapse and cancerous possibility, it causes great harm on the quality of patients’ lives and work. Currently, the general treatment of western medicine for chronic refractory wounds is early debridement, infection control, application of appropriate wound dressings. It is a single processing means. Some special treatment, such as the clinical application of exogenous growth factors, tissue engineering skin is not extensively used in clinical, the overall effect in promoting chronic wound healing are not ideal. The method of TCM stage diagnosis and treatment, the body overall governance combined with local external treatment does have efficacy in promoting chronic wound healing. Large number of studies are expanded to explore mechanism of traditional Chinese medicine action in chronic wound healing process. The basis of the research of wound healing mechanism and evaluation of wound healing drugs is to establish animal models in line with the clinical disease process and the main factors of impacting wound healing. Chronic wound healing model should reflect the complexity of the pathogenesis of chronic dermal wounds, multiple factors, chronic wound infection and chronic inflammation. In the study for replication of animal model should seize one or several of the main factors affecting the replication of the model.The study showed that oxidative stress is an important mechanism for the delay wound healing. Oxidative stress is a state of decline in a body from oxidation and anti-oxidation homeostasis. It is caused by that free radicals increases, and (or) the body or tissue antioxidant capacity decreases. Many cells can generate oxygen free radicals in varying degrees in the wound microenvironment, the amount of free radicals can play a beneficial role in wound healing, excessive free radicals leading to tissue damage is not conducive to wound healing. Further study the mechanism of oxidative stress on wound healing, for the treatment of chronic wounds to provide a broader ideas and approaches.Objective Through the use of skin defects and Epirubicin intervention composited, a chronic wound model in oxidative stress state has been established.MethodsThe rats were divided into normal group (no skin defects), the simple group (skin defects), model group, simple group and model group rats were punched a diameter of1.5cm hole on the back playing with a special hole punch, forming a open wound of full-thickness skin defect. On this basis, model group rats were injected epirubicin (2mg/ml) of0.15ml in the wound edge skin. The changes were observed in rat wounds in general, calculated wound area and wound healing rate on the day3,6,11,20, drawn on the day3,7,14,22.1/2in wound tissue was performed with10%formalin-fixed, paraffin-embedded, sliced, with HE, Masson staining to observe the wound histological changes.1/2wound tissue is made to homogenates. Blooding in the abdominal aorta in rats to make serum. Biochemical methods used to measure the level of SOD, MDA, H2O2of skin homogenate and serum. For statistical analysis, comparison between the two groups.ResultModel group and the skin defect group, the wound healing time, to20days simple group wound has almost healed wounds of the model group to the first28-30days of basic healing. At the same time, the wound healing rate of model group was significantly lower than the skin defect group (P<0.01). Observation of the simple group wound tissue slice shows many inflammatory cells in3rd day, visible new capillaries in dermis and fibroblast distribution in7th day, a large number of fibroblasts and new collagen in wound tissue in14th day, the new cuticle formation and new collagen arranged in neat rows in22nd day. Compared with the simple group, model group wound sustained infiltration of inflammatory cells from3rd day to22nd day, as a small number of fibroblasts, a small number of new collagen, arranged in disorder. Determination of each group of rat skin homogenate and serum SOD, MDA,, H2O2, level, in the third and seventh day, the model group and the skin defect group compared with the normal group, SOD activity decreased significantly (P<0.01), MDA, the level of H2O2significantly increased (P<0.01). Model group shows the lower the activity of SOD, MDA, H2O2, a higher level, with significant differences (P<0.05) compared with skin defect group.14th day, the simple group SOD activity and MDA level of H2O2was compared with the normal group without significant difference (P>0.05), model group is still a significant difference (P<0.01), the activity of SOD is lower than the normal group of MDA, H2O2, higher than the normal group.ConclusionThe superposition method using the complex factors of skin defects interfere with epirubicin to establish a rat dermal wound model used in the experiment, the method can be successfully copied oxidative stress refractory wound model in rats. The model is applied to the study of Chinese medicine to promote wound healing mechanism through the oxidative damage. |
PDF Full Text Request