[Research advances of the roles of sphingosine-1-phosphate in acute lung injury].

Sphingosine-1-phosphate (S1P) is the main metabolite produced in the process of phospholipid metabolism, which can promote proliferation, migration, and apoptosis of cells, and maintain the barrier function of vascular endothelium. The latest researches showed that S1P can alleviate acute lung injury (ALI) and the inflammation caused by ALI, while the dosage of S1P is still needed to be considered. Mesenchymal stem cells (MSCs) have been a emerging therapy with potential therapeutic effects on ALI because of their characteristics of self-replication and multi-directional differentiation, and their advantages in hematopoiesis, immune regulation, and tissue repair. S1P can promote differentiation of MSCs and participate in immune regulation, while MSCs can regulate the homeostasis of S1P in the body. The synergistic effect of S1P and MSC provides a new treatment method for ALI. This article reviews the production and biological function of S1P, receptor and signal pathway of S1P, the therapeutic effects of S1P on ALI, and the research advances of S1P combined with MSCs in the treatment of ALI, aiming to provide theoretical references for the development of S1P targeted drugs in the treatment of ALI and the search for new combined treatment schemes for ALI.

[Mechanism of lung injury of rats induced by inhalation of white smoke from burning smoke pot].

Objective: To explore mechanism of lung injury of rats induced by inhalation of white smoke from burning smoke pot. Methods: Forty-eight Sprague Dawley rats were divided into control group (n=12) and injury group (n=36) according to the random number table. Rats in injury group were placed in smoke-induced injury experimental equipment fulled with white smoke from burning smoke pot for 5 minutes to make lung injury, and rats in control group were placed in smoke-induced injury experimental equipment fulled with air for 5 minutes to make sham injury. Six rats in injury group at post injury hour (PIH) 6, 24, and 72 and six rats in control group at PIH 72 were collected to observe pathological changes of lung tissue and pathological score of rats in the two groups by hematoxylin-eosin staining, to detect expression of nuclear factor-κB (NF-κB) p65 mRNA in lung tissue of rats by reverse transcriptional polymerase chain reaction, and to detect content of tumor necrosis factor α (TNF-α), interleukin 1ß (IL-1ß), and IL-6 in lung tissue of rats by enzyme-linked immunosorbent assay. Data were processed with one-way analysis of variance and t test. Results: At PIH 72, lung tissue structure of rats in control group was clear and complete, with no inflammatory cell infiltration. At PIH 6, there was edema, hemorrhage, and inflammatory cell infiltration in lung tissue of rats in injury group. At PIH 24, edema, hemorrhage, and inflammatory cell infiltration in lung tissue of rats in injury group aggravated. At PIH 72, area of edema in lung tissue of rats in injury group was enlarged, with obvious hemorrhage and inflammatory cell infiltration. At PIH 6, 24, and 72, pathological score of lung tissue of rats in injury group was (3.43±0.86), (5.39±0.93), and (9.99±0.84) points, respectively, obviously higher than that of rats in control group at PIH 72 [(2.11±0.20) points, t=3.659, 8.450, 22.355, P<0.05]. As time post injury prolonged, pathological scores of lung tissue of rats in injury group were significantly increased (F=121.244, P<0.01). At PIH 6, 24, and 72, expression of NF-κB p65 mRNA in lung tissue of rats in injury group was 15.5±4.3, 25.9±1.8, 30.9±3.5 respectively, significantly higher than that of rats in control group at PIH 72 (7.8±0.8, t=4.315, 20.445, 14.408, P<0.01). As time post injury prolonged, expression of NF-κB p65 mRNA in lung tissue of rats in injury group gradually increased (F=32.691, P<0.01). At PIH 6, 24, and 72, content of TNF-α, IL-1ß, and IL-6 in lung tissue of rats in injury group was significantly higher than that of rats in control group at PIH 72, respectively (t=7.650, 8.968, 6.827, 6.726, 8.978, 3.460, 5.420, 13.289, 16.438, P<0.01). At PIH 24, content of TNF-α and IL-1ß in lung tissue of rats in injury group was higher than that of rats in the same group at PIH 6 and 72, respectively (t=3.409, -2.549, 4.047, -4.100, P<0.05). At PIH 24 and 72, content of IL-6 in lung tissue of rats in injury group was respectively higher than that of rats in the same group at PIH 6 (t=8.273, 9.711, P<0.05). Conclusions: After inhaling white smoke from burning smoke pot, rats are inflicted with lung injury by increasing expression of NF-κB p65 mRNA and content of TNF-α, IL-1ß, and IL-6, and induce pathological changes of edema, hemorrhage, and inflammatory cell infiltration of lung tissue.

[Treatment of patients with different degree of acute respiratory distress syndrome caused by inhalation of white smoke].

Objective: To summarize the treatment experience of patients with different degree of acute respiratory distress syndrome (ARDS) caused by inhalation of white smoke from burning smoke bomb. Methods: A batch of 13 patients with different degree of ARDS caused by inhalation of white smoke from burning smoke bomb, including 2 patients complicated by pulmonary fibrosis at the late stage, were admitted to our unit in February 2016. Patients were divided into mild (9 cases), moderate (2 cases), and serious (2 cases) degree according to the ARDS Berlin diagnostic criteria. Patients with mild and moderate ARDS were conventionally treated with glucocorticoid. Patients with severe ARDS were sequentially treated with glucocorticoid and pirfenidone, and ventilator-assisted breathing, etc. were applied. The vital signs, arterial oxygenation index, changes of lung imaging, pulmonary ventilation function, general condition, and the other important organs/systems function were timely monitored according to the condition of patients. The above indexes were also monitored during the follow-up time of 10-15 months post injury. Data were processed with SPSS 18.0 statistical software. Results: (1) The symptoms of respiratory system of patients with mild and moderate ARDS almost disappeared after 3 days' treatment. Their arterial oxygenation index was decreased from post injury day 1 to 4, which almost recovered on post injury day 7 and completely recovered one month post injury. The symptoms of respiratory system of patients with severe ARDS almost disappeared at tranquillization condition 1-3 month (s) post injury. Their arterial oxygenation index was decreased from post injury day 3 to 21, which gradually recovered 1-3 month (s) post injury and was normal 15 months post injury. (2) Within 24 hours post injury, there was no obvious abnormality or only a little texture enlargement of lung in image of chest CT or X-rays of patients with mild and moderate ARDS. One patient with moderate ARDS had diffuse patchy and ground-glass like increased density shadow (pulmonary exudation for short) at post injury hour 96. Chest iconography of all patients with mild and moderate ARDS showed no abnormalities 10 months post injury. Both lungs of each of the two patients with severe ARDS showed obvious pulmonary exudation at post injury hours 45 and 75, respectively. One patient with severe ARDS showed no abnormality in chest image 10 months post injury, but there was still a small mesh-like increased density shadow in double lobes with slight adhesion of pleura in the other patient with severe ARDS 15 months post injury. (3) All patients showed severe restrictive hypoventilation when admitted to hospital. Pulmonary ventilation function of patients with mild and moderate ARDS recovered to normal one month post injury, and they could do exercises like running, etc. Pulmonary ventilation function of one patient with severe ARDS recovered to normal 6 months post injury, and the patient could do exercises like running, etc. The other patient with severe ARDS showed mild restrictive hypoventilation 15 months post injury and could do exercises like rapid walking, etc. (4) The condition of all mild and one moderate ARDS patients was better on post injury day 3, and they were transferred to the local hospital for subsequent treatment and left hospital on post injury day 21. One patient with moderate ARDS healed and left hospital on post injury day 29. Patients with severe ARDS healed and left hospital on post injury day 81. During the follow-up time of 10-15 months post injury, the other important organs/systems of all patients showed no abnormality, and there was no adverse reaction of glucocorticoid like osteoporosis, femoral head necrosis, or metabolic disorder. Two patients with severe ARDS did not have any adverse reaction of pirfenidone like liver function damage, photosensitivity, anorexia, or lethargy. Conclusions: Early enough and uninterrupted application of glucocorticoid can significantly reduce the ARDS of patients caused by inhalation of white smoke from burning smoke bomb. Sequential application of glucocorticoid and pirfenidone can effectively treat pulmonary fibrosis at the late stage.