摘要
目的观察雌激素对皮瓣缺血再灌注损伤的保护作用，初步研究c—Jun氨基末端激酶（c—JunN—terminal kinase，JNK）通路与雌激素保护作用的相关性。方法取40只Wistar大鼠建立大鼠腹部皮瓣缺血再灌注损伤模型，随机分为健康对照组（A组）、缺血再灌注损伤组（B组）、雌激素组（C组）、JNK抑制剂组（D组）。术后第七天观察各组皮瓣大体情况，测量皮瓣成活面积并计算成活率，HE染色观察各组皮瓣组织学改变，测定皮瓣组织中JNK、p-JNK、丝裂原活化蛋白激酶磷酸酶-5（MKP-5）的表达。分析皮瓣成活率与JNK表达量的相关性。结果c组和D组皮瓣生长良好，皮瓣成活率较B组明显提高，皮瓣组织学改变较B组轻。C组、D组皮瓣州K、P—JNK表达量较B组明显降低，c组、D组州K负性调控因子MKP-5表达明显较B组增高。结论雌激素能明显改善皮瓣缺血再灌注损伤，提高皮瓣成活率，其机制可能是雌激素通过调控JNK通路发挥了对皮瓣的缺血再灌注损伤保护作用。
Objective To observe the protective effect of estrogen against ischemia reperfusion injury in axial flaps, and investigate the role of the c-Jun N-terminal kinase signaling pathway in estrogen＇ s protective effect. Methods An ischemia reperfusion injury model in the abdominal flap was created in 40 Wistar rats that were randomly divided into 4 groups： control （group A）, ischemia reperfusion injury （group B）, estrogen （group C） and JUN inhibitor （group D）. Seven days postoperatively, gross observation of the flap, measurement of flap survival area and calculation of flap survival rate were carried out. The flap tissues were harvested for hematoxylin-eosin staining to observe histological changes, and for Western blot to quantify JNK, p-JNK and MKP-5 expression. The relationship between flap survival and JNK expression was analyzed. Results Flaps in groups C and D grew well. Flap survival rates in these two groups were significantly higher than that in group B, while pathological changes were milder. Expressions of JNK and p-JNK were significantly lower in flaps of groups C and D than in flaps of group B, while expression of JNK negative regulator MKP-5 was the opposite. Conclusion Estrogen can significantly improve the ischemia reperfusion injury in flaps and increase flap survival rate. The potential mechanism of estrogen＇s protective effect can be through regulating Jun N-terminal kinase signaling pathway.
出处
《中华手外科杂志》
CSCD
北大核心
2016年第1期62-65,共4页
Chinese Journal of Hand Surgery
