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目的探讨红霉素在早产鼠高氧肺损伤中对白细胞介素6(IL-6),IL-8及γ-谷氨酰半胱氨酸合成酶(γ-GCS)的干预作用。方法 96只早产新生SD大鼠生后1 d分为四组:Ⅰ组空气暴露+生理盐水、Ⅱ组空气暴露+红霉素、Ⅲ组高氧暴露+生理盐水、Ⅳ组高氧暴露+红霉素,每组各24只。四组分别于高氧或空气暴露后1、7、14 d处死取肺组织做病理学检查。采取双抗体夹心酶联免疫吸附试验分析肺组织匀浆细胞因子IL-6、IL-8和γ-GCS的水平,并采取半定量逆转录聚合酶链反应测定γ-GCS mRNA的表达。结果Ⅰ、Ⅱ组肺组织无明显病理改变,Ⅲ组肺泡炎性改变及水肿较Ⅳ组更为明显。Ⅳ组γ-GCS水平在7、14 d较Ⅲ组降低,但是γ-GCS mRNA表达较γ-GCS mRNA均明显增强(P均<0.05)。Ⅲ组1、7、14 d IL-6及IL-8水平较Ⅰ组均显著增强(P均<0.05)。Ⅳ组IL-6水平在1、7、14 d与Ⅲ组比较,差异均有统计学意义(P均<0.05),而IL-8水平仅在7、14 d较Ⅲ组明显下降(P均<0.05)。结论氧化爆发诱导的炎症介质IL-6及IL-8参与高氧肺损伤发病过程,红霉素可抑制其释放,影响γ-GCS活性从而提高谷胱甘肽抗氧化能力。
Objective To investigate the effects of erythromycin on interleukin 6 (IL-6), IL-8 and γ-glutamylcysteine synthetase (γ-GCS) in hyperoxia-induced lung injury in premature rats. Methods 96 premature newborn SD rats were divided into four groups 1 d after birth: air exposure + saline, group Ⅱ air exposure + erythromycin, group Ⅲ hyperoxia exposure + saline, group Ⅳ hyperoxia exposure + red Mycotoxin, each group of 24. Four groups were sacrificed at 1, 7, 14 days after exposure to hyperoxia or air, respectively, to take lung tissue for pathological examination. The levels of IL-6, IL-8 and γ-GCS in lung homogenates were detected by double antibody sandwich enzyme-linked immunosorbent assay. The expression of γ-GCS mRNA was determined by semi-quantitative reverse transcription polymerase chain reaction. Results There was no obvious pathological changes in lungs of group Ⅰ and group Ⅱ, and the changes of alveolitis and edema in group Ⅲ were more obvious than that of group Ⅳ. The level of γ-GCS in group Ⅳ was lower than that in group Ⅲ at 7 and 14 days, but the expression of γ-GCS mRNA was significantly higher than that of γ-GCS (all P <0.05). The levels of IL-6 and IL-8 in group Ⅲ at 1, 7, 14 d were significantly higher than those in group Ⅰ (all P <0.05). The levels of IL-6 in group Ⅳ were significantly lower than those in group Ⅲ at 1, 7 and 14 days (all P <0.05), while the levels of IL-6 were significantly lower at 7 and 14 days <0.05). Conclusions The inflammatory mediators IL-6 and IL-8 induced by oxidative burst are involved in the pathogenesis of hyperoxia-induced lung injury. Erythromycin can inhibit its release and affect the activity of γ-GCS, thereby enhancing the antioxidant capacity of glutathione.