论文部分内容阅读
目的探讨经体表创伤后肾脏组织中缺氧诱导因子-1α(HIF-1α)、过氧化物酶体增殖物激活受体γ(PPAR-γ)表达的变化,及创伤后肾脏损伤与修复的作用机制。方法采用自由落体生物撞击仪撞击大鼠脊肋区复制创伤动物模型。实验大鼠分为5组,包括非创伤对照组,创伤后1、6、12、24 h组。采用免疫组织化学方法进行HIF-1α、PPAR-γ染色。结果肾脏创伤后1、24 h HIF-1α表达增强,分布于皮质远曲小管、肾盏旁小管、髓质小管;6、12 h表达减弱,局限于肾盏旁小管、髓质外带小管。各组间比较差异有统计学意义(P<0.05)。PPAR-γ1、24 h呈阳性表达,分布于髓质小管上皮细胞;6、12 h呈阴性表达,各组间比较差异有统计学意义(P<0.05)。结论 HIF-1α、PPAR-γ可能参与了肾脏创伤后缺血、缺氧、再生、修复的过程。
Objective To investigate the changes of expression of hypoxia inducible factor-1α (HIF-1α) and peroxisome proliferator-activated receptorγ (PPAR-γ) in kidneys after traumatic skin injury and the effects of traumatic renal injury and repair Mechanism. Methods Free-falling biological impactor was used to impact the rat’s rib cage region to copy the wound animal model. The experimental rats were divided into five groups, including non-trauma control group, 1,6,12,24 h after trauma group. HIF-1α and PPAR-γ were stained immunohistochemically. Results The expression of HIF-1α was increased at 1 and 24 h after trauma in the kidneys. The distribution of HIF-1α was mainly located in the distal convoluted tubules, the parabronchial tubules and the medullary tubules. The expression of HIF-1α was weakened at 6 and 12 h. The difference between each group was statistically significant (P <0.05). PPAR-γ1 was positive for 24 h and distributed in medullary tubule epithelial cells. The expression of PPAR-γ1 was negative at 6 and 12 h, with significant difference between groups (P <0.05). Conclusions HIF-1α and PPAR-γ may participate in the process of ischemia, hypoxia, regeneration and repair after kidney trauma.