Protectin DX promotes epithelial injury repair and inhibits fibroproliferation partly via ALX/PI3K signalling pathway.

Acute respiratory distress syndrome/acute lung injury (ARDS/ALI) is histologically characterized by extensive alveolar barrier disruption and excessive fibroproliferation responses. Protectin DX (PDX) displays anti-inflammatory and potent inflammation pro-resolving actions. We sought to investigate whether PDX attenuates LPS (lipopolysaccharide)-induced lung injury via modulating epithelial cell injury repair, apoptosis and fibroblasts activation.

[Spectroscopy research on cholesterol in hypercholesterolemia serum].

The cholesterol with different concentration in hypercholesterolemia serum was studied by the method of spectroscopy technology. The absorption and fluorescence spectra of normal human serum and hypercholesterolemia serum were obtained respectively; the spectral characteristic of each sample and the difference between two kinds of samples were discussed too. The results indicate that the absorption and fluorescence spectra of hypercholesterolemia serum are different from those of normal human serum.

[Changes of thioredoxin mRNA level in neurons insulted by sodium azide].

Oxidative stress has been considered to be associated with many neurodegenerative diseases, while mitochondrial damage is one of the important reasons that aggravate oxidative stress. Sodium azide (NaN3) is a specific inhibitor of mitochondrial cytochrome c oxidase (COX), which can be used to mimic neuronal damage induced by mitochondrial deficiency. In this experiment, the neurotoxic effects of NaN3 on cultured primary neurons were detected by means of cell viability measurement (MTT assay) and morphological observation, and an in vitro model of neuronal injury induced by NaN3 were established.

[Construction and identification of recombinant adenovirus vector containing thioredoxin reductase gene].

Aim: To construct recombinant adenovirus vector containing human thioredoxin reductase (TR) gene and to explore the correlation between antioxidant activity of TR and the degenerative neuropathy.

Methods: Full length TR cDNA was obtained from recombinant plasmid pGEM-TR via digestion with Apa I and Not I and was cloned into pShuttle vector and pShuttle-TR was recut with I-Ceu I and PI-Sce I. Fragment containing TR gene and CMV promoter was inserted into E1 and E3 deficient adeno-X virus DNA, and then the recombinant adenovirus vector was transfected into HEK 293 cells through lipofectamine and identified by PCR.

[Changes of thioredoxin mRNA level in neurons with mitochondrial dysfunction insulted by H2O2].

Oxidative stress and mitochondrial deficiency have been considered to be associated with the mechanisms of many neurodegenerative diseases. Sodium azide (NaN3) is a special inhibitor of mitochondrion cytochrome c oxidase (COX), which can be used to mimic neuronal damage induced by mitochondrial deficiency. In this experiment, the neurotoxic effects of H2O2 on primary cultured neurons and NaN3-induced mitochondrial dysfunctional neurons were detected by means of cell viability measurement (MTT) and analyzed through morphological observation.