Accidents, Occupational ; Acute Disease ; Adult ; Humans ; Male ; Sulfuric Acid Esters ; poisoning

This study is to determine the preventive effect and mechanism of targeting IL-17A on pulmonary inflammation and fibrosis after acute lung injury. Mice were treated with anti-IL-17A antibody on the day 7 and sacrificed on the day 14 after bleomycin lung injury. The pulmonary inflammatory status and the deposition of collagen were measured by HE and Sirius stains staining. The contents of hydroxyproline and collagen were measured by using commercial kits. The survival rate of mice was calculated by Kaplan-Meier methods. The inflammatory cytokines in bronchoalveolar lavage fluid were measured by ELISA and the expressions of inflammation-related molecules were detected by Western blotting assay. Targeting of IL-17A could prevent the development of lung inflammation, decrease collagen deposition and the contents of hydroxyproline, and protect against the development of pulmonary fibrosis, which together led to an increase in the animal survival. Moreover, blocking IL-17A decreased the expression ofpro-fibrotic cytokines such as IL-17A, TGF-beta1 and IL-13; increased the expression of anti-fibrotic or anti-inflammatory factors such as IFN-gamma, COX-2, 5-LOX, 15-LOX. Indeed, IL-17A antagonism suppressed the activation of pro-inflammatory p65NF-kappaB but enhanced the activation of pro-resolving p50NF-kappaB. In conclusion, that blockade of IL-17A prevents the development of pulmonary fibrosis from acute lung injury, is because blocking IL-17A may prevent acute inflammation converting to chronic inflammation.

Objective To investigate the mechanism underlying the protective effect of hyperbaric oxygen (HBO) in secondary spinal cord injury (SCI). Methods Models of acute SCI were established in 96 SpragueDawley rats using Allen's dropping weight technique. The rats were then divided into a HBO group, a high pressure nitrogen normal oxygen group, a normal pressure oxygen group and a normal pressure air group. The injured spinal cords were sampled for morphological studies at the 1 st, 3rd, 7th and 14th day after injury. Apoptotic cells were labeled using the TUNEL technique, and the expression of caspase-3 was detected. The neurological functionality of the spinal cord was assessed by open field locomotor evaluation ( the BBB score). Results The expression of caspase3 in the HBO group decreased significantly more than in the other groups after injury. The number of TUNEL-positive cells was significantly lower in the HBO group as well. Neurological function improved significantly after HBO therapy. Conclusions HBO can down-regulate the expression of caspase-3 and inhibit cell apoptosis in rats after SCI.The protective effect of HBO was related with the oxygen level.

Objective To explore the effect and mechanism of L-arginine on fetal growth restriction by observing the expression of Bcl-2 and Bax in placenta.Methods Sixty patients with FGR were chosen,among which 30 cases who were treated with conventional ways were as convention group,and the other 30 cases who were treated with L-arginine were as L-arginine group.The birth weight and perinatal fetus outcome were detected.The central tissue of placenta got within 10 min after delivery were fixed by 100 g/L formaldehyde and embed by pa-raffin wax to observe the expression of Bcl-2 and Bax using immunohistochemistry.SPSS 11.5 software was used to analyze the data.Results Compared with convention group,the birth weight of L-arginine group was higher(P

G protein-coupled receptor 119 (GPR119) has been a promising target for the treatment of type 2 diabetes. It can not only directly promote insulin secretion, but also indirectly increase insulin secretion by stimulating the release of glucose-dependent GIP/CLP-1 without causing hypoglycemia. The remarkable advantages of small molecule GPR119 agonists make it one of the research hotspots for the development of type 2 diabetes drugs. This article reviews the anti-diabetic small molecules based on the GPR119 target in the past five years.

Angiotensins ; analysis ; Animals ; Animals, Newborn ; Biomarkers ; analysis ; Endothelin-1 ; analysis ; Hypertension, Pulmonary ; drug therapy ; metabolism ; physiopathology ; Lung ; chemistry ; pathology ; Magnesium Sulfate ; pharmacology ; Nitric Oxide Synthase ; analysis ; Nitric Oxide Synthase Type II ; Swine ; Vasomotor System ; chemistry

Background To suppress vascular endothelial growth factor (VEGF) is a researching hot topic for the treatment and prevention of retinal neovascularization.Some detectable efficacy of VEGF small interference RNA (VEGF siRNA) in anti-tumor neovascularization has been well-known.But relevant study on VEGF siRNA on retinal neovascularization is seldom.Objective Present study was to investigate the inhibiting effect of VEGF siRNA on retinal neovascularization.Methods The 48 clean C57BL/6J mice aged 7-day-old were randomly divided into normoxia group,hypoxia control group,vector group and VEGF siRNA group and 12 mice for each.Hypoxia models were established by raising the pups with mother mice in the airtight oxygen-cabin for 5 days.The lipofectamineTM 2000 (LF2000)-mediated vector plasmids or VEGF siRNA recombinant plasmids were then injected intravitreally in 12 12-day-old pup mice respectively.The animals were sacrificed in 1 week after intravitreal injection,and the numbers of vascular endothelial cell nuclei extending beyond the internal limiting membrane (ILM) were counted by hematoxylin-eosin stain.The expressions of VEGF protein and mRNA in retina were assayed by immunoinfluorescence technique and RT-PCR.Results The numbers of vascular endothelial cell nuclei extending beyond the ILM were 0.19±0.09,24.89±2.03,23.65±2.15 and 8.83±1.12 in normoxia group,model control group,vector group and VEGF siRNA group separately,showing significant decrease in VEGF siRNA group compared with model control group or vector group (q=5.67,q=4.97,P＜0.01).RT-PCR revealed that VEGF mRNA was faintly expressed in mouse retina in normoxia group.However,in model control group and vector group,the level of VEGF mRNA was 52.3 times and 36.7 times more than that of normoxia group respectively and only 3.5 times in VEGF siRNA group,presenting a inhibitory rate of 43.39% of VEGF siRNA on VEGF.Immunofluorescence showed that the expression of VEGF was weaker in normoxia group and strong positive response in model control group and vector group,but the expression intensity of VEGF protein was significantly weaker in VEGF siRNA group.Conclusion VEGF siRNA recombinant plasmids can efficiently inhibit retinal neovascularization in oxygen-induced retinopathy mouse model through intravitreal injection.

The effects of pretreatment methods of Jerusalem artichoke tubers on microbial lipids fermentation with an oleaginous yeast strain Rhodosporidium toruloides Y4 were investigated in shaking flask culture.The yeast strain accumulated substantial amount of lipids using either purple-or white-skinned Jerusalem artichoke tubers as sole carbon and energy source.When cells were cultured on the extracted juice or the acidhydrolysate,cellular lipid content reached 40%(w/w),while cultured on the pulp,the white-skinned tubershadhigher lipid productivity,yielding 12.1 g lipids per100 g dried tubers.Major fatty acid constituents of microbial lipids were those contained 16-and 18-carbon atoms based on GC analysis,which is quite similar to traditional vegetable oil.Microbial lipids prepared from Jerusalem artichoke can be applied to biodiesel production.

Objective To study the expression of intermediate-conductance-Ca~(2+)-activated K~+ (IKCa1)channels in endometrial cancer and its role in regulating proliferation of endometrial cancer cells. Methods Western blot and RT-PCR were used to examine the expression of IKCa1 channels in 13 normal endometrial specimens and 25 endometrial cancer specimens;and RNA interference(RNAi),[ ~3H ] thymidine incorporation,and inhibitor of IKCa1 channel were used to explore the role of IKCa1 channels in regulation of proliferation of endometrial cancer cells HEC-1A.Results The expression rate and level of IKCa1 mRNA in endometrial carcinoma(84%,0.89?0.52)were higher than in normal endometria(8%, 0.14?0.12;P

Anti-cancer drug bleomycin (BLM) can cause acute lung injury (ALI) which often results in pulmonary fibrosis due to a failure of resolving acute inflammatory response. The aim of this study is to investigate whether toll-like receptor (TLR) 2 mediates BLM-induced ALI, inflammation and fibrosis. BLM-induced dendritic cells (DCs) maturation was analyzed by flow cytometry and cytokine secretion was detected by the ELISA method. The expression and activity of p38 and ERK MAPK were determined with Western blotting. The roles of TLR2 in ALI, inflammation and fibrosis were investigated in C57BL/6 mice administered intratracheally with BLM. The results demonstrated that BLM-administered mice had higher expression of TLR2 (P<0.001) and its signaling molecules. Blocking TLR2 significantly inhibited the maturation of DCs and reversed BLM-stimulated secretion of cytokines in DCs, such as IL-6 (P<0.001), IL-17 (P<0.05) and IL-23 (P<0.05). TLR2 inhibition attenuated BLM-induced increase of inflammatory cells in bronchoalveolar lavage fluid (BALF), and reversed the immunosuppressive microenvironment by enhancing TH1 response (P<0.05) and inhibiting TH2 (P<0.001), Treg (P<0.01) and TH17 (P<0.01) responses. Importantly, blocking TLR2 in vivo significantly protected BLM-administered mice from pulmonary injury, inflammation and fibrosis and subsequently increased BLM-induced animal survival (from 50% to 92%). Therefore, TLR2 is a novel potential target for ALI and pulmonary fibrosis.