NF-κB在大鼠急性肺损伤模型肺组织中的表达及N-乙酰半胱氨酸的影响

NF-κB expression in lung tissue of (acute) lung injury rat model and the influence by antioxidant N-acetylcysteine

目的 :检测NF κB在LPS诱导的急性肺损伤 (ALI)肺组织中的表达 ,以及N 乙酰半胱氨酸 (NAC)对ALI的抑制作用。方法 :采用免疫组化染色 (ABC法 )和Westernblot,检测NF κB在急性肺损伤大鼠气道和肺组织中的表达 ,以及NAC干预后活性NF κB表达的变化。结果 :正常对照组大鼠气道黏膜上皮和肺间质中 ,仅见少量散在的NF κB核阳性细胞 ;而LPS诱导ALI后 ,气道黏膜、肺间质、肺泡腔及血管内皮细胞中NF κB核阳性的细胞明显增多 (P <0 .0 1)。NF κB核阳性反应细胞主要为气道黏膜上皮细胞、浸润的炎症细胞、肺泡上皮细胞和血管内皮细胞。NAC治疗组NF κB核阳性细胞较LPS诱导的ALI组及对照组均明显减少 (P <0 .0 1)。Westernblot的结果显示 ,LPS诱导的ALI后不同时间点 ,NF κB的表达不同 ,于急性肺损伤 3h达高峰。各时间点NF κB的表达均较正常对照组高。结论 :LPS诱发的大鼠急性肺损伤的气道和肺组织内NF κB的表达增加 ,肺组织内的多数细胞参与了NF κB的激活。NAC可通过抑制NF

AIM: To observe the NF-κB expression in the lung tissue of LPS-induced acute lung injury(ALI) rat model and the influence of N-acetylcysteine (NAC) on NF-κB expression. METHODS: The expression of NF-κB in lung tissue in ALI rat model and the influence of NAC on NF-κB expression were detected by immunohistocheimical (ABC) staining and Western blot. RESULTS: There were a small amount of sporadic NF-κB cells in airway epithelium and interstitium in normal control group. In contrast, nuclear NF-κB expression-positive cells increased obviously in airway mucosa, lung interestium, alveolar cavity and vascular wall of ALI rats. NF-κB^+ cells were mainly airway mucosa epithelial cells, infiltrating inflammation cells, alveolar epithelial cells, and vascular endothelial cells. The NF-κB expression-positive cells in NAC therapy group notably decreased compared with ALI group and control group(P<0.01). Western blot analysis showed that the expression of NF-κB was different at various time points, reaching the peak at 3 h and then decreased (P<0.01) after LPS induced lung injury. CONCLUSION: In LPS induced acute lung injury rat model, the NF-κB nuclear expression increased obviously in airway mucosa, lung interestium and alveolar cavity. Most cells in lung tissue participated in the activation of NF-κB. NAC could alleviate inflammation by inhibiting activation of NF-κB.