Aim To investigate the immune regulation of IL-23 fusion gene and the correlation between its biological function and the airway inflammation in asthma during pregnancy. Methods The eukaryotic expression plasmid,which was constructed to express the IL-23p40 + p19 double subunit,was used to transform E.coilBL21 bacteria,and the expression products,which were induced by IPTG,were purified and detected by SDS-PAGE and Western blot. The transfection,mediated by recombinant protein,was identified by fluorescence microscopy and plasmid's Western blot,while DNA binding activity of nuclear proteins was measured by gel electrophoresis. To evaluate the impact of foreign protein in vivo,mouse serum inflammatory cytokines levels and inflammation injury in lung tissue were measured by ELISA method and HE staining. The CD4+T cell subset's proportion of mononuclear cells in peripheral blood was verified by flow cytometry. Results The results showed that soluble exogenous recombinant protein,which was obtained successfully,had the ability of trans-membrane transport and could effectively mediate EGFP into the target cells. Its stable expression and transcriptional activity were higher than those of simple plasmid's effect. The specific binding between GST/pCEP4-IL-23 and plasmid DNA formed macromolecular complexes,which could decrease the mobility of gel. The combined effect with LPS significantly increased the IL-17A levels in serum(P 0. 05) and the inflammation reaction in lung tissue of sensitized mice. Mean while,it also reduced the IFN-γ,Foxp3 level in serum,promoted the activation of IL-4 and IL-17A,and then increased the ratio of Th2/Th1and Th17/Treg(P 0. 05). Conclusions The recombinant IL-23 protein is pathogenic,and it adjusts the inflammation of asthma in pregnancy. The immune imbalance of CD4+T subsets affects the immune tolerance of pregnant body and the development of asthma during pregnancy.

Intracellular levels of ubiquitous transduction signal cyclic adenosine 3',5'-monophosphate( cAMP) and cyclic guanosine 3',5'-monophosphate( cGMP) are partly determined by the hydrolysis by phosphodiesterases( PDEs). So far,the superfamily of PDE is composed of at least 11 isoforms and each family is characterized with unique cellular distribution,expression,regulation mode and inhibitor sensitivity,and PDEs are considered to be involved in a variety of pathological processes, such as inflammation,asthma,depression,and erectile dysfunction,etc. Currently,these characteristics draw PDEs more and more attention as great targets for drugs. In this review,the basic biochemical properties,cellular regulation,expression pattern,physiological functions and inhibitors of different PDE isoforms will be briefly discussed.

Aim: To explore the underlying mechanism of hyperthyroidism induced by subcutaneous injection of L-levothyroxine sodium and and intervention effects of Liuwei Dihuang pills on sprague dawley rats via serum metabolomics. Methods: After rats were injected with L-levothyroxine sodium at a dosage of 35 μg·(100 g)-1 every day for 1 week,and then Liuwei dihuang pills(LDPs) were treated at a dose of 4.7 g·kg-1 for 3 consecutive weeks.The serum samples for rats were obtained after the treatment of LDPS and the metabolic profiles of serum were obtained with ultra performance liquid chromatography coupled with time-of-flight mass spectrometry(UPLC-QTOF-MS). Results: The levels of oxaloacetic acid,Dihydroxyacetone phosphate(DHAP),ethyl glucuronide,triglyceride,lysophospholipids and cholesterol were significantly increased in the model group as compared to the normal rats.Moreover,these levels could be regulated to be close to normal after the treatment of LDPS. Conclusions: There is severe disturbance in the tricarboxylic acid cycle as well as sugar and lipid metabolism for hyperthyroidism rats.LDPS can exhibite obvious effects on the treatment of hyperthyroidism.Serum metabonomics analysis reveals the changes of metabolites traits during the treatment of LDPS,thus providing a supplementary evaluation method of LDPS in the treatment of hyperthyroidism.

Aim To explore the role of inhibitor of apoptosis proteins(IAP) in regulating the sensitivity of gastric cancer cells to tumor necrosis factor-related apoptosis-inducing ligand(TRAIL)-induced apoptosis.Methods Apoptotic cells were determined by the propidium iodide method using flow cytometry.The activation of caspase-3 and PARP cleavage were conducted by Western blot analysis.Expressions of XIAP,Survivin,cIAP1 and cIAP2 before and after treatment with TRAIL were also measured by Western blot analysis.Results TRAIL induced apoptosis in gastric cancer cells.BGC-823 cells were more sensitive to TRAIL than SGC-7901 cells.Caspse-3 activation and PARP cleavage were detected early after exposure to TRAIL.IAP family members were constitutively overexpressed in the two cell lines.The expression of XIAP was significantly downregulated in BGC-823 cells,compared with that in SGC-7901 cells,after TRAIL treatment.The expression of Survivin and cIAP1 remained unchanged.The expression of cIAP2 was slightly lowered in the two cell lines.Conclusions TRAIL-induced apoptosis of gastric cancer cells appears to be determined at the level of the effector caspase-3.XIAP protects gastric cancer cells from TRAIL-indued apoptosis.