Icariin reduces LPS-induced acute lung injury in mice undergoing bilateral adrenalectomy by regulating GRα.

In the present study, we established the acute lung injury (ALI) model of mice with adrenal insufficiency, and to investigate the possible mechanism by which Icariin (ICA) reduces lipopolysaccharide (LPS) -induced ALI in mice undergoing bilateral adrenalectomy by regulating glucocorticoid receptor α (GRα). ALI of BALB/c mice with adrenal insufficiency was induced by LPS and bilateral adrenalectomy (ADX). The pathological and morphological changes in lung tissues were observed, the levels of corticosterone, IL-6, and TNF-α in serum and lung tissues by ELISA. The levels of GRα, IL-6, TNF-α, NF-κB p65, Stat3, and c-Jun in lung tissues were detected by RT-qPCR and Western Blotting, GRα activity was blocked by GRα antagonist RU486. It was found that the dual intervention of LPS and ADX had further aggravation the downregulation of GRα and upregulation of NF-κB p65, c-Jun, Stat3, and IL-6 and TNF-α, ICA enhanced the expression of GRα in lung tissues and inhibited the expression of NF-κB p65, c-Jun, Stat3, IL-6, and TNF-ɑ, thereby reducing ALI. However, RU486 could partially counteract the protective effect of ICA on lung injury and its downregulating effect on various inflammatory transcription factors and inflammatory cytokines. In conclusion, ICA reduces ALI in mice undergoing bilateral ADX by regulating GRα, and no inhibitory effect on hypothalamic pituitary adrenal (HPA) axis.

Differential protein expression profiling by iTRAQ-2D-LC-MS/MS of rats treated with oxaliplatin.

Clinical application of oxaliplatin, a platinum-based chemotherapeutic agent, in cancer, especially colorectal cancer, is widely used. However, oxaliplatin-induced peripheral neurotoxicity (OIPN) has a high incidence, and to date, there have been few detailed studies on pathogenesis and treatment mechanisms. The present study was performed by using a proteomic approach to explore protein expression profiling of rats treated with oxaliplatin by multiplex isobaric tags for relative and absolute quantification labeling and two-dimensional liquid chromatography-tandem mass spectrometry. There were 74 proteins that showed different expression in sciatic nerve between control rats and OIPN model rats, with 53 upregulated proteins and 21 downregulated proteins detected in OIPN groups compared with control groups. On the basis of Gene Ontology clustering, these proteins were associated with biological processes (eg, muscle contraction, muscle system process, and skeletal muscle contraction), cellular component (eg, myofibril, contractile fiber, and contractile fiber part) and molecular function (structural constituent of muscle, hydro-lyase activity, and calcium ion binding). On the basis of Kyoto Encyclopedia of Genes and Genomes pathway database, these proteins were associated with African trypanosomiasis, malaria, nitrogen metabolism, etc. Real-time polymerase chain reaction, Western blot as well as immunohistochemistry analysis was performed to examine the expression of partially differential protein. In conclusion, our study establishes a protein expression profile of oxaliplatin-induced rats and mechanisms leading to OIPN development, and will be useful for developing novel diagnostic biomarkers and aiding in the prevention and control of OIPN.

MicroRNA-29a Promotes Pancreatic Cancer Growth by Inhibiting Tristetraprolin.

BACKGROUND/AIMS: The microRNA (miR) 29 family has been studied extensively for its involvement in several diseases, and aberrant expression of its members is associated with tumorigenesis and cancer progression. Here, we examined the role of miR-29a in pancreatic cancer and the involvement of tristetraprolin (TTP). METHODS: We monitored miR-29a and TTP expression in pancreatic cancer by qRT-PCR and western blotting. The effect of miR-29a on pancreatic cancer was determined through MTT assay and migration assay. The results were validated in the tumorigenesis model. RESULTS: We found that miR-29a was up regulated in pancreatic tumor tissues and cell lines and positively correlated with metastasis. Ectopic expression of miR-29a increased the expression of pro-inflammatory factors and epithelial-mesenchymal transition (EMT) markers, through down regulating TTP. TTP was down regulated in tumor tissues, and its ectopic expression decreased cell viability and migration in vitro, inhibited tumor growth and the EMT phenotype in vivo, and reversed the effect of miR-29a on tumor cell proliferation and invasion in vitro and in vivo. CONCLUSION: Our results suggest that miR-29a acts as an oncogene by down regulating TTP and provide the basis for further studies exploring the potential of miR-29a and TTP as biomarkers and targets for the treatment of pancreatic cancer.

Percutaneous needle decompression in treatment of malignant small bowel obstruction.

AIM: To investigate the efficacy and safety of percutaneous needle decompression in the treatment of malignant small bowel obstruction (MSBO). METHODS: A prospective analysis of the clinical data of 52 MSBO patients undergoing percutaneous needle decompression was performed. RESULTS: Percutaneous needle decompression was successful in all 52 patients. Statistically significant differences were observed in symptoms such as vomiting, abdominal distension and abdominal pain before and after treatment (81.6% vs 26.5%, 100% vs 8.2%, and 85.7% vs 46.9%, respectively; all P < 0.05). The overall significantly improved rate was 19.2% (11/52) and the response rate was 94.2% (49/52) using decompression combined with nasal tube placement, local arterial infusion of chemotherapy and nutritional support. During the one-month follow-up period, puncture-related complications were acceptable. CONCLUSION: Percutaneous needle intestinal decompression is a safe and effective palliative treatment for MSBO.