AIM: To explore the expressions and significance of angiopoietin-2 (Ang-2) and tyrosine kinase with immunoglobulin and epidermal growth factor homology domains-2 (Tie-2) receptors in a rat model of acute lung injury (ALI). METHODS: Wistar rats (n=42) were divided into control group (n=12) and cecal ligation and puncture (CLP) group (n=30). Control group underwent sham operation, and CLP group underwent cecal ligation and puncture to make the model of ALI. 12 h after sham operation or CLP, 6 rats in each group were killed, and arterial blood gas analysis and lung coefficient were tested. The expressions of Ang-2 and Tie-2 receptors in lung tissue were observed by immunohistochemical method. Blood samples of the rest rats were collected from vena caudalis, and Ang-2 levels were measured by enzyme linked immunosorbent assay (ELISA). The mortality rate in each group within 36 h was compared. The lung architecture was observed under microscope. RESULTS: The lung architecture in control group was clear and intact. Alveolar septum was thicker, blood capillary was congested, and neutrophils and macrophages were infiltrated in the lung tissue in CLP group. Tie-2 receptors were expressed in bronchial epithelial cells, smooth muscle cells and endothelial cells in control group. Besides the similar expression as control group, high expression of Tie-2 on neutrophils and macrophages in CLP group was observed. In the adhesion location of Tie-2 receptors positive inflammatory cells, there was stronger staining in endothelial cells. Ang-2 was expressed in smooth muscle cells, bronchial epithelial cells and endothelial cells in control group. The Ang-2 level in CLP group were higher than that in control group [(8.14±1.74) μg/L vs (4.63±0.49) μg/L, P<0.01], and the Ang-2 level of dead rats was higher than that of survival rats within 36 h in CLP group [(8.95±1.61)μg/L vs (6.80±0.96)μg/L, P<0.01]. Oxygen partial pressure in control group was lower (P<0.01) and lung coefficient was higher (P<0.01) than that in CLP group. CONCLUSION: Ang-2 and Tie-2 receptors may participate in the pathophysiology of ALI, and Ang-2 level is correlated with mortality.

Objective To explore the endovascular therapeutic strategy for multiple occlusive lesions of aorta and iliac-femoral arteries, and to discuss the technical skill as well as the clinical significance. Methods A total of 8 patients with multiple occlusive lesions of aorta and iliac-femoral arteries were enrolled in this study. Preoperative CT angiography and MR angiography were performed in all the 8 patients. The lesions included complete occlusion of abdominal aorta below renal artery level (n = 2), distal abdominal aorta occlusion (n = 4), distal abdominal aorta stenosis (n = 1), distal abdominal aorta membranous occlusion (n = 1), and diseased iliac artery (n = 12), external iliac artery (n = 8), femoral artery (n = 1) and popliteal artery (n = 2). Endovascular interventional management, including opening channel, thrombolysis, balloon dilation, stent implantation, etc. was carried out via different routes. The results were analyzed. Results After endovascular interventional management the abdominal aorta was completely reopened in all the 8 patients. Of 12 diseased iliac arteries, 9 were successfully reopened by interventional treatment and the remaining 3 were not treated. All the diseased external iliac arteries were opened up. The involved femoral artery and popliteal arteries were not treated. The patients were followed up for 1 -12 months. During the follow-up period, ischemic symptoms of the lower limb disappeared in 5 patients and were obviously improved in 2 patients. Recurrence of thrombotic occlusion was observed in one case, which returned to normal after transcatheter thrombolysis therapy. Conclusion For the treatment of multiple occlusive lesions of aorta and iliac-femoral arteries, endovascular interventional management is safe, simple and effective with fewer complications. The ischemic symptoms of the lower limb can be significantly improved.

Objective:To investigate the expression of long non-coding RNA (Lnc RNA) RP5-919F19 in gastric cancer tissues and its correlation with gastric cancer invasion and metastasis.Methods:Non-tumor gastric mucosa (more than 3cm away from the cancer tissue) and gastric adenocarcinoma tissues were collected from Jan. 2020 to Jan. 2022 in our hospital. TRIzol kit was used to extract total RNA from cells and tissues, and reverse transcription kit was used to reverse transcribed RNA into cDNA. Quantitative real-time PCR kit was used for quantitative analysis. SGC-7901 and AGS human gastric cancer cells were used to construct RP5-919F19 knockdown and overexpression models. CCK-8 assay was used to confirm cell proliferation, and Transwell invasion assay was used to confirm the invasion ability of gastric cancer cells.Results:The expression of RP5-919F19 was detected in 79 cases of gastric cancer tissues and adjacent normal tissues, and it was found that the relative expression of RP5-919F19 in gastric cancer tissues was 1.51±0.05 significantly higher than that of 0.82±0.04 in adjacent normal tissues ( P<0.05) . The levels of RP5-919F19 in patients with different pathological conditions were compared and analyzed. The results showed that there were statistically significant differences in RP5-919F19 expression in patients with different TNM stages, distant metastasis, lymph node metastasis and different depth of invasion ( P<0.05) . There was no significant difference in RP5-919F19 expression among patients with different tumor sizes, ages and genders ( P>0.05) . AGS gastric cancer cells were transfected with RP5-919F19 overexpression plasmid and control plasmid, and the efficiency of RP5-919F19 was detected. The results showed that the expression level of RP5-919F19 in the overexpression group was 1.83±0.14 higher than that of 0.82±0.05 in the control group ( P<0.05) . SGC-7901 gastric cancer cells were transfected with RP5-919F19 knockout vector and control vector, and the efficiency of RP5-919F19 was detected. The results showed that the expression level of RP5-919F19 in the knockout group was 0.42±0.07 lower than that of 0.89±0.08 in the control group ( P<0.05) . CCK-8 was used to detect the proliferation ability of gastric cancer cells. The results showed that the proliferation ability of AGS cells in RP5-919F19 overexpression group was significantly increased compared with that of the control group at 24 and 48h after culture ( P<0.05) . However, the proliferation ability of SGC-7901 cells in RP5-919F19 knockdown group was lower than that in the control group at 24 h and 48 h ( P<0.05) . Transwell invasion assay showed that the invasion and migration abilities of AGS cells in RP5-919F19 overexpression group were higher than those in the control group ( P<0.05) , and the invasion and migration abilities of SGC-7901 cells in RP5-919F19 knockout group were lower than those in the control group ( P<0.05) . Western blot showed that compared with control cells, the expression of MMP-2 and MMP-9COPS7A proteins in down-regulated Lnc RNA RP5-919F19 SGC-7901 cells was decreased. Conclusion:The expression of LncRNA RP5-919F19 is abnormally increased in gastric cancer tissues, and the increased expression of RP5-919F19 can promote the proliferation and metastasis of gastric cancer cells.

Objective To validate the mechanism of Mori Cortex-Lycii Cortex(MCLC)in intervening acute lung injury(ALI)based on network pharmacology,molecular docking combined with animal experiments.Methods The TCMSP database was used to obtain the active components of MCLC;the SwissTargetPrediction database was used to predict the targets of active components;the GeneCards database and DisGeNET database were used to collect the disease targets of ALI;the key targets were screened by constructing a PPI network,and the key targets were subjected to GO and KEGG pathway enrichment;a drug-component-target-pathway network was constructed using Cytoscape software;AutoDock and PyMOL software were used to validate the molecular docking of some of the compounds and targets;LPS was used to establish a mouse model of ALI for experimental validation,and experimental validation was performed to main targets and pathways.Results Totally 44 active components of MCLC and 138 action targets were obtained;26 potential targets of MCLC intervention in ALI were obtained,mainly TNF,EGFR,NFKB1,MPO,TNFRSF1A,NOX4,etc.,and the key pathways were MAPK signaling pathway,IL-17 signaling pathway,NF-κB signaling pathway,etc.;molecular docking results showed that the core active components of MCLC and the main targets had strong binding activities;animal experiments showed that MCLC at medium and high dosages could effectively improve the lung histopathological damage in ALI mice,decrease the contents of IL-6 and TNF-α in serum(P<0.01),and increase IL-10 content(P<0.01);MCLC inhibited protein expressions of EGFR,PI3K,AKT,NF-κB p65 in lung tissue(P<0.01).Conclusion MCLC may intervene ALI by components such as quercetin and buddleoside,acting on targets including EGFR and TNF,through ulti-pathways of EGFR/PI3K/NF-κB signaling pathway,etc.