AIM To investigate whether pioglitazone can protect cortical neurons from lipopolysaccharides(LPS)-induced neurotoxicity and the mechanisms responsible for this protective effect. METHODS After 7 d cultures，cultured cortical neurons were incubated with LPS 10 mg·L~(-1) for 4-24 h with or without other drugs. In co-incubation experiments, other drugs were added to the neurons 30 min or 1 h prior to incubation with LPS. The cell viability was assessed by MTT assay. The neuronal apoptosis was quantified by scoring the percentage of cells with apoptotic nuclear morphology after Hoechst 33258 staining. The cultured cells were then fixed on the 7th day and immunocytochemically stained with phosphorylated JNK1 antibody. The protein expressions of active caspase 3 and phosphorylated JNK1 were measured by Western blot. Nitric oxide (NO) generation was measured by Griess method. RESULTS The decrease of cell viability and the increase of apoptotic cells in cultured cortical neurons were observed incubated with LPS for 24 h compared with the normal controls. The cell viability of cortical neurons was decreased from (100.0±10.9)% in the normal control group to (72.3±2.1)% in the LPS-treated group and the apoptotic cell percentages were increased from (11.5±4.2)% in the normal control group to (39.5±8.2)% in the LPS group. LPS induced the increases in phospho-JNK1, active caspase 3 expression, and NO generation. Pioglitazone 0.01, 0.1 and 1 μmol·L~(-1), respectively inhibited LPS-induced decrease in cell viability and increase of apoptotic morphology, active caspase 3 expression in cultured neurons. In LPS+pioglitazone 1 μmol·L~(-1) group, cell viability was （97.8±9.7）%, the apoptotic cells percentage was (20.6±5.0)%, NO generation (6.8±1.3)μmol·L~(-1). Furthermore, pioglitazone also inhibited LPS-induced the increase in JNK1 phosphorylation and NO generation. JNK inhibitor SP600125 5 μmol·L~(-1) significantly inhibited LPS-induced neurotoxicity, cell viability was increased from (72.3±2.1)% to (109.8±11.8)%, the apoptotic cells percentage from (39.5±8.2)% decreased to (19.1±4.8)%, NO generation from （21.1±5.0）μmol·L~(-1) decreased to（4.0±1.3）μmol·L~(-1). The PPARγ antagonist GW9662 10 μmol·L~(-1) did not reverse the effects of pioglitazone. In LPS+pioglitazone 1 μmol·L~(-1)+GW9662 10 μmol·L~(-1) group, cell viability was (90.7±6.9)%, the apoptotic cells percentage was (23.4±4.1)%, and NO concentration was (5.8±0.7)μmol·L~(-1). CONCLUSION Pioglitazone protects cortical neurons against LPS insult at least via inhibiting JNK activity and NO generation, but not PPARγ activation.

Aim To investigate whether pioglitazone has protective effect against glutamate induced neurotoxicity in cultured cortical neurons and its possible molecular mechanisms underlying pioglitazone's neuroprotective effects.Methods The cortical neurons were taken from newborn rats and used for experiments 7 days after culture.The neurons were randomly divided into control group;glutamate group; glutamate+piogli-tazone group;glutamate+SP600125 group;SP600125 group.Cell viability was determined by MTT.The morphology change of neurons was observed under a fluorescence microscope with fluorescence dye Hoechst 33258.Immunostaining was used to investigate the expression of phospho-ATF2 in neuronal cells.Western blot was performed to investigate the protein level of phospho-JNK1 and total JNK1.Results Pioglitazone markedly reduced the damage of cortical neurons caused by glutamate.Pioglitazone also significantly inhibited glutamate induced up-regulation of phospho-JNK1 protein level and phospho-ATF2 expression.SP600125, an inhibitor of JNK, antagonized the toxicity induced by glutamate.Conclusions Pioglitazone can protect cultured cortical neurons from glutamate induced damage.The protective effect of pioglitazone appears to be associated with inhibiting the c-Jun N-terminal protein kinase signaling pathway.

Objective To explore the effects of salidroside(SAL)on high glucose-induced epithelial-mesenchymal transition in ARPE-19 cells and its mechanism.Methods The appropriate glucose concentration for stimulating ARPE-19 cell proliferation was determined to be 50 mmol·L-1 using the MTT method.ARPE-19 cells were divided into the normal control group(Control group)(cultured with 5 mmol·L-1 D-glucose and 45 mmol·L-1 mannitol),high glucose group(HG group)(cultured with 50 mmol·L-1 glucose),HG+low SAL group,HG+medium SAL group,and HG+high SAL group,with low,medium,and high SAL concentrations of 20 μmol·L-1,80 μmol·L-1,and 320 μmol·L-1,respective-ly.After 4 hours of SAL pretreatment,50 mmol·L-1 glucose was added to treat cells for 48 hours.The cell proliferation rate was detected using the MTT method;the cell migration activity was detected using the scratch experiment;the expres-sion levels of α-smooth muscle actin(α-SMA)and Vimentin in cells were measured using the immunofluorescence;the protein expression levels of α-SMA,Vimentin,fibronectin(FN),collagen type Ⅰ(Col Ⅰ),E-Cadherin,transforming growth factor-β1(TGF-β1),p-Smad2 and p-Smad3 in cells were measured using Western blot.Results Compared with the Control group,the proliferation rate and wound healing percentage of ARPE-19 cells in the HG group increased;the relative expression levels of α-SMA,Vimentin,FN,and Col Ⅰ proteins in the cells increased;the relative expression level of E-cad-herin protein in the cells decreased;the relative expression levels of TGF-β1,p-Smad2,and p-Smad3 proteins in the cells increased,and the differences were statistically significant(all P＜0.01).Compared with the HG group,the proliferation rate and wound healing percentage of ARPE-19 cells in the HG+low SAL group,HG+medium SAL group,and HG+high SAL group decreased,the relative expression levels of α-SMA,Vimentin,FN,Col Ⅰ,TGF-β1,p-Smad2,and p-Smad3 pro-teins in the cells decreased in a concentration dependent manner,while the relative expression level of E-cadherin protein increased in a concentration dependent manner,and the differences were statistically significant(all P＜0.05).Conclu-sion SAL can reduce the proliferation and migration ability of high glucose-induced ARPE-19 cells and intervene in their epithelial-mesenchymal transition process.This may be related to SAL's inhibition of the TGF-β/Smads signaling pathway in ARPE-19 cells.

Objective To explore the development of disaster nursing in undergraduate courses . Methods Measures were done in writing program , course design , textbook writing , determining the content , theoretical teaching and experimental teaching .Results In 2012, 51 among 60 students (85.00%) selected the course of disaster nursing .In 2013, 40 among 60 students ( 66.67%) selected the course of disaster nursing.During the two years of course development , 75.83% students selected the disaster nursing courses . The class hour increased from 24 to 30 .The textbook of disaster nursing was edited and published as the nursing teaching materials of the twelfth five-year plan .Conclusions It is necessary to develop the disaster nursing in undergraduate education .We recommend promoting the disaster nursing in medical colleges and universities .