Abstract

To study the molecular mechanism of immune regulation of toll-like receptor 9/myeloid differentiation factor 88 signal pathway in neonatal acute lung injury. Fifty-one newborn mice were divided into control group (n=17), model group (n=17) and experimental group (n=17). The model of acute lung injury in neonatal mice was established by intraperitoneal injection of kanamycin. The mice in the control group and model group were fed and treated normally, while the mice in the experimental group were treated with toll-like receptor 9 inhibitor chloroquine to inhibit toll-like receptor 9/myeloid differentiation factor 88 signal pathway. Compared with the model group, the degree of lung injury in the experimental group was alleviated after administration of toll-like receptor 9 inhibitor and the pathological score of lung tissue in the experimental group was lower than the model group, but higher than the control group. Compared with the model group, the toll-like receptor 9 and myeloid differentiation factor 88 messenger ribonucleic acid in the experimental group decreased. The toll-like receptor 9 and myeloid differentiation factor 88 in the model group model group was up-regulated after acute lung injury, while toll-like receptor 9 and myeloid differentiation factor 88 in the experimental group was decreased. Compared with the model group, the expression of toll-like receptor 9 and myeloid differentiation factor 88 protein in the experimental group decreased. Compared with the model group, the content of superoxide dismutase in the experimental group increased and the content of malondialdehyde decreased, the difference was significant. Compared with the model group, the levels of tumor necrosis factor-alpha and interleukin-6 in the lung tissue of the experimental group were down-regulated. The results show that toll-like receptor 9/myeloid differentiation factor 88 signaling pathway is a potential therapeutic target for inflammatory response in neonates with acute lung injury.