糖尿病大鼠皮肤伤口愈合过程中结缔组织生长因子的表达

背景：结缔组织生长因子表达在糖尿病伤口愈合过程中的变化及意义少见报道。目的：观察链脲佐菌素诱导的糖尿病模型大鼠复合创伤修复过程中结缔组织生长因子表达的变化及意义。方法：将Wistar大鼠随机分成正常对照组和模型组,3周后将各组动物复合背部1.3cm2全厚皮切除形成伤口。结果与结论：链脲佐菌素诱发的糖尿病模型大鼠伤口愈合明显延迟,创伤后第4,8,12和16天创面愈合率明显低于正常对照组（P〈0.01）。术后第8天,糖尿病组大鼠肉芽组织成熟度和新生血管形成指标得分均低于正常对照组（P〈0.01）。正常对照组的结缔组织生长因子蛋白表达呈时间递增趋势,而糖尿病组的结缔组织生长因子表达在整个创面愈合过程的后期（第12天后）均明显低于正常对照组（P〈0.01）。结果提示,糖尿病大鼠皮肤伤口愈合后期创面组织结缔组织生长因子表达相对正常对照组减少可能是导致创面愈合迟缓的重要原因之一。

Expression of connective tissue growth factor in the skin wound of diabetic rats

BACKGROUND：Studies about connective tissue growth factor （CTGF） expression in the wound healing in diabetes mellitus are rare.OBJECTIVE：To study CTGF expression during wound healing in diabetic rats induced by streptozotoein.METHODS：Fifty SD male rats were randomly divided into control group and model group.50 mg/kg STZ were given intraperitoneally to model rats.After 3 weeks,a round skin of 1.3 cm2 was excised on all dorsal back of rats.The healing time and healing rate were observed according to re-epithelization.Routine HE staining was made to calculate the granulation tissue thickness and angiogenesis at different time points.Western blotting was used to detect the expression of protein of CTGF in the skin at those time points.RESULTS AND CONCLUSION：The healing time in the model group was （25.06±2.11） days,significantly longer than （16.17±1.88） days in the control group （P〈0.01）.The healing rates in the model group were significantly less than that in the control group at days 4,8,12 and 16 （P〈0.01）.The amount of granulation tissue thickness and angiogenesis in the model group were significantly less than those in the control group on days 8,12 and 16,respectively （P〈0.01）.The expression of CTGF protein in the wound of the control group increased with time,the values were much higher than that in the model group after day 12 （P〈0.01）.Streptozotocin （STZ）-induced diabetic rats impairs wound healing which is possibly caused by the relative reduce of CTGF expression in the wound compared to non-diabetic rats.The biology of wound healing and the pathobiology of impaired wound healing in diabetes are emphasized to illustrate how these future molecular therapeutics are intended to counteract disease pathology and promote normal wound repair.