Application values of thromboelastography (TEG) in dynamic monitoring of coagulation parameters of sepsis patients were investigated. Eighty-one patients with sepsis who were admitted to the ICU department of the General Hospital of Ningxia Medical University from April 1, 2015 to December 31, 2015 were collected. Clinical data of the patients were collected. Data were compared using 5 grouping methods: i) the 81 patients were divided into the sepsis group (n=45) and sepsis shock group (n=36); ii) patients were divided into two groups: group A (APACHE II score ≤13, n=51); group B (APACHE II score >13, n=30); iii) according to Disseminated Intravascular Coagulation Diagnosis Integral System (CDSS), patients were divided into non-disseminated intravascular coagulation (DIC) group (CDSS <7 points) and DIC group (CDSS ≥7 points); TEG indexes were compared between the two groups; iv) correlation between TEG indexes and Sequential Organ Failure Assessment (SOFA) scores was analyzed; v) patients were divided into survival group and non-survival group and correlations between TEG indicators and prognosis were analyzed. At 6 h after ICU entry, compared with sepsis group, R value and K time were significantly increased, LY30 was also increased, while MA value, coagulation index (CI), and α angle were significantly decreased in the septic shock group (P<0.05). At 6 h after ICU entry, compared with sepsis group, R value and K time were significantly increased, while MA value, CI, and α angle were significantly decreased in the septic shock group (P<0.05). Compared with the non-DIC group, the DIC group had prolonged K time, decreased α angle, increased R value, and decreased CI and MA value (P<0.05). With increase of SOFA scores, R value and K value increased significantly, and α angle, MA value, and CI decreased significantly (P<0.05). According to TEG, platelet function and fibrinogen function of DIC patients were significantly reduced, and the body showed hypocoagulability.

Reducing inflammation can effectively relieve acute lung injury (ALI). Objective. To test whether keratinocyte growth factor‐2 (KGF‐2) can reduce oleic acid‐induced inflammation in ALI of rats and explore its possible mechanism. Methods. 45 Sprague‐Dawley rats were randomly divided into control group, ALI group, and ALI + KGF‐2 group. The animal model of acute lung injury was established by injecting 0.1 mL/kg oleic acid into the tail vein of rats. Rats in the control group were injected with equal volume of normal saline (NS). Each group needs pretreatment 72 hours before the preparation of the acute lung injury model. The control group and ALI group were instilled with 5 ml/kg NS through the airway, and the same amount of KGF‐2 was instilled in the ALI + KGF‐2 group. It takes 8 hours to successfully prepare the ALI model. Observe the pathological changes of lung tissue through light microscopy, ultrastructural changes through electron microscopy, and the lung wettability/dry weight (w/d) ratio and lung permeability index (LPI). By detecting changes in inflammatory factors in lung tissue and changes in the number of BALF cells, the changes in inflammation in each group were observed. The expressions of Wnt5a, β‐catenin, and APC in lung tissue were detected by immunohistochemistry and Western blot. The changes of key proteins in Wnt/β‐catenin signaling pathway in the lung tissue of each group were observed. Result. Compared with the ALI group, after KGF‐2 pretreatment, the degree of lung injury was reduced, the expression of inflammatory factors was reduced, and the number of red blood cells and white blood cells in BALF was reduced. It can also be observed that the expression of Wnt5a, β‐catenin, and APC, a key protein in the Wnt/β‐catenin signaling pathway, is reduced. The analysis showed that the number of inflammatory factors, red blood cells, and white blood cells in BALF was positively correlated with the expression of Wnt5a, β‐catenin, and APC. Conclusion. KGF‐2 may reduce the inflammatory response in ALI induced by oleic acid by regulating key proteins in the Wnt/β‐catenin signaling pathway.

Objective. The aim of this study was to examine the role of keratinocyte growth factor-2 (KGF-2) in oleic acid-induced acute lung injury (ALI) in rats. Methods. Forty-five healthy adult male Sprague Dawley rats were divided into 3 groups. Rat ALI model was established by injection of 0.01 mL/kg oleic acid into the tail vein. Rats in the control group were injected with the same amount of normal saline (NS). In the ALI + KGF-2 group, 5 mg/kg of KGF-2 was instilled into the airway of rats 72 hours before the model preparation, and the control group and the ALI model group were instilled with the same amount of NS. The lung permeability index (LPI) and lung wet/dry weight (W / D) ratios were measured 8 hours after the model preparation. The permeability of pulmonary microvascular endothelium was evaluated by Evans blue leakage test. Histopathological changes were observed under light microscope and the ALI pathology score (LIS) was calculated. Ultrastructural changes of lung tissue were observed under electron microscope. The apoptosis was detected by TUNEL assay. The expression of Claudin-5, ZO-1, and VE Cadherin in lung tissue was qualitatively and quantitatively analyzed by immunohistochemistry, Western Blot, and qRT-PCR, respectively. Results. The ALI model group had severe lung injury and obvious pathological changes, including alveolar septal thickening and inflammatory cell infiltration. TUNEL assay showed that the apoptosis of ALI group was significantly increased. The LIS score, lung W/D ratio, LPI, and Evans blue leakage were significantly higher than those in the control group; electron microscopy showed that the alveolar-capillary barrier was severely damaged in the ALI group. Compared with the control group, the expression of Claudin-5, ZO-1, and VE cadherin in the lung tissue of the ALI model group was significantly attenuated. After pretreatment with KGF-2, the degree of lung tissue damage was significantly reduced and the pathological changes were significantly improved. TUNEL assay showed that the apoptosis of ALI group was decreased. Lung W/D ratio, LPI, and Evans blue leakage decreased; electron microscopy showed that the alveolar-capillary barrier of ALI group recovered significantly. Compared with the ALI model group, the expression of Claudin-5, ZO-1, and VE cadherin in the lung tissue of the KGF-2 pretreatment group increased. Conclusion. The results indicate that KGF-2 may attenuate oleic acid-induced ALI in rats by maintaining the pulmonary microvascular endothelial barrier, which is an effective ALI preventive measure.