谷氨酰胺抑制早产高氧肺损伤大鼠肺组织的炎症反应及其机制

Glutamine inhibits the inflammation in preterm rats with lung injury induced by hyperoxia and its mechanism

目的研究谷氨酰胺对早产高氧肺损伤大鼠肺部炎症反应的影响及机制。方法制备早产高氧肺损伤大鼠模型,给予谷氨酰胺处理。利用Diff-Quik染色检测大鼠支气管肺泡灌洗液中炎症细胞聚集情况,HE染色观察早产高氧肺损伤大鼠肺组织的炎症变化,TUNEL染色观察早产高氧肺损伤大鼠肺组织的细胞凋亡情况,ELISA检测支气管肺泡灌洗液(BALF)中白细胞介素1β(IL-1β)和肿瘤坏死因子α(TNF-α)水平,Western blot法检测肺组织中丝裂原活化蛋白激酶磷酸酶1(MKP-1)、丝裂原活化蛋白激酶(MAPK)及胞质磷脂酶A2(cPLA2)的磷酸化水平。结果谷氨酰胺处理可以抑制肺部炎症反应和细胞凋亡,减少IL-1β和TNF-α的表达,促进MKP-1的磷酸化,抑制MAPK的激活和cPLA2磷酸化,减轻肺部炎症,缓解早产高氧大鼠肺组织肺炎症损伤。结论谷氨酰胺通过调节MKP-1/MAPK信号通路抑制早产高氧肺损伤大鼠肺部炎症反应。

Objective To investigate the effect of glutamine on the preterm hyperoxia-induced lung inflammation injury of rat models. Methods The rat model of lung injury induced by preterm hyperoxia was prepared and treated with glutamine.Diff-Quik staining was used to detect the aggregation of inflammatory cells in the bronchoalveolar lavage fluid(BALF),and HE staining was used to observe the inflammation of lung tissues. TUNEL staining was performed to detect the cell apoptosis in the lung tissues,and ELISA to test the levels of IL-1β and tumor necrosis factor α(TNF-α) in BALF. The phosphorylation of mitogen-activated protein kinase phosphatase-1(MKP-1),mitogen-activated protein kinase(MAPK) and cytosolic phospholipase A2(cPLA2) in the lung tissues were detected by Western blotting. Results Glutamine alleviated lung inflammation response and cell apoptosis,and reduced the levels of IL-1β and TNF-α in the inflammatory lung tissues of premature rats. Meanwhile,glutamine promoted the phosphorylation of MKP-1,and inhibited the activation of MAPK and cPLA2. Conclusion Glutamine inhibits pulmonary inflammation in preterm hyperoxia-induced lung injury rat models via regulating MKP-1/MAPK signaling pathway.