Protective effects of ulinastatin on rats with acute lung injury induced by lipopolysaccharide.

We aimed to evaluate the protective effects of ulinastatin (UTI) on rats with acute lung injury induced by lipopolysaccharide (LPS) via the Toll like receptor 4 (TLR4)/myeloid differentiation factor 88 (MyD88)/nuclear factor-kappa B (NF-κB) signaling pathway. Forty-eight male Wistar rats were randomly divided into model, control, dexamethasone (DXM) and UTI groups. The body weight loss ratio and wet-to-dry weight ratio (W/D) of lung tissue were calculated at 10 h. The permeability of pulmonary vascular endothelium was detected by Evans blue method. Tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6) and IL-1ß levels in bronchial lavage fluid were detected by enzyme-linked immunosorbent assay. Total cells and neutrophils were counted by microscopy. TLR4, MyD88 and NF-κB expressions were detected by Western blotting. Compared with model group, DXM and UTI groups had significantly higher body weights and lower W/D values (P<0.05). In DXM and UTI groups, the lung tissue structure was close to normal, inflammatory cell infiltration was alleviated, and hematoxylin-eosin staining scores were significantly lower than that of model group (P<0.05). Compared with model group, the concentrations of Evans blue, IL-1ß, IL-6 and TNF-α levels, and protein expressions of TLR4, MyD88 and NF-κB in DXM and UTI groups decreased significantly (P<0.05). UTI inhibits LPS-induced activation of the TLR4/MyD88/NF-κB signaling pathway, thereby alleviating inflammatory response and protecting against lung injury.

Hinokinin alleviates high fat diet/streptozotocin-induced cardiac injury in mice through modulation in oxidative stress, inflammation and apoptosis.

Type 2 diabetes, a global health concern has been considered as major risk factor for cardiovascular diseases. Hinokinin, an emerging bioactive lignin, is reported to show wide range of pharmacological activities. However, the protective role and mechanisms of Hinokinin against type 2 diabetes-mediated cardiotoxicity are still remains unknown. An experimental type 2 diabetic mice model was created by treating animals with high fat diet for four weeks and intraperitoneal injection of streptozotocin (35 mg/kg body weight). Post-type 2 diabetic induction, animals orally treated with Hinokinin (20 or 40 mg/kg body weight) for six weeks. The type 2 diabetic mice exhibited a rise in blood glucose level as well as glycated hemoglobin (HbA1c %), decrease in weekly body weights, decrease in food intake, reduction in absolute heart weight, fall in serum insulin level with altered lipid profile and cardiac functional damage. Diabetic mice treated with Hinokinin attenuated hyperglycemia, dyslipidemia and cardiac dysfunction. In addition, Hinokinin ameliorated histological alterations, fibrosis and glycated proteins in HFD/STZ-induced mice. Type 2 diabetic condition in mice exacerbated oxidative stress, inflammatory status and apoptosis. Hinokinin treatment significantly assuaged oxidative stress, inflammation and apoptosis and elevated antioxidant defenses in diabetic heart. The underlying mechanisms for such mitigation involved the modulation of Nrf2/Keap1/ARE pathway, MAPKs (JNK, p38 and ERK 1/2) and TLR4/MyD88/NF-κB mediated inflammatory pathways and mitochondrial-dependent (intrinsic) apoptosis pathway. In conclusion, the results of this study provided clear evidence that Hinokinin protects against HFD/STZ (type 2 diabetes)-induced cardiac injury by alleviating oxidative stress, inflammation and apoptosis.

[Experience of Interventional Thrombolysis Therapy for Massive Pulmonary Thrombosis Embolism after Video-assisted Thoracoscopic Surgery for Lung Cancer].

BACKGROUND: Pulmonary thrombosis embolism (PTE) is one of the most severe complications of perioperative radical mastectomy. Massive PTE is often accompanied by shock and hypotension which is characterized by rapid progression and high mortality. There is no standard for the treatment of these patients, which is thoracic surgery, and it is a critical issue in the thoracic surgeons. This article summarizes and analyzes the treatment of two patients with high-risk PTE at the early stage of postoperative lung cancer in our hospital. In addition, we discusses the diagnosis and treatment strategies of these cases to provide a reference for the thoracic surgeons. METHODS: We presented two patients with high-risk PTE at the early stage after thoracic surgery for radical surgery in our hospital back in 2017. One case was treated with intravenous venous interventional thrombolysis, and the other was treated with thrombolysis alone. The treatment effect of two patients and the complications during the treatment has been recorded to detail and summarized. RESULTS: Both patients were female who aged 66 and 61 years old. The time point of pulmonary embolism was 48 h and 45 h after operation, and the time of interventional thrombolysis was 70 minutes and 50 minutes after onset respectively. After 120 minutes and 100 minutes, the drainage after interventional thrombolysis was 4,690 mL and 520 mL respectively. The hospitalization time after thrombolysis was 21 days and 14 days respectively. There was no obvious complication through a follow-up of 6 months. CONCLUSIONS: Early postoperative acute massive pulmonary embolism in lung cancer should be treated with pulmonary interventional thrombolysis as soon as possible. Compared with intravenous thrombolysis, pulmonary interventional thrombolysis shows accuracy, easy controlling of dosage, fast curative effect and low bleeding risk.

MicroRNA-30c functions as a tumor suppressor via targeting SNAI1 in esophageal squamous cell carcinoma.

BACKGROUND: Aberrant expression of miRNAs was involved in tumor initiation, progression and metastasis in multiple cancers. Many kinds of microRNAs in esophageal squamous cell carcinoma (ESCC) have been researched, whereas miR-30c has not been included. METHODS: Firstly, we explored the expression of miR-30c in ESCC tissue and serum samples and its relations to the survival. To further investigate its effects on ESCC cells, we completed a series of experiments. We detected the effects of ectopic miR-30c expression on the proliferation, migration and invasion of ESCC cells in vitro. We identified the target role of SNAI1 in ESCC using Dual-luciferase reporter assay and western blot assay. RESULTS: The results showed miR-30c was significant down-regulated in ESCC tissues and cell lines. Clinically, we found lower miR-30c expression was significantly correlated with worse ESCC progression and survival. Also we clarified that miR-30c suppressed cell proliferation, invasion and epithelial to mesenchymal transition (EMT) of ESCC cell lines. What's more, we figured out that miR-30c inhibits ESCC biological behaviors and EMT progress by directly binding to the 3'-UTR of SNAI1. CONCLUSION: This study provides new insight into the mechanism responsible for the development of human ESCC. Therefore, miR-30c could be a promising biomarker and a therapeutic target for ESCC in the future.