[Objective]To investigate the effect of human umbilical cord mesenchymal stem cells on infected state of human alve?olar type Ⅱ epithelial cells.[Methods]Human alveolar type Ⅱ epithelial cells A549(1×105/mL)2 mL and PA(3×104 CFU/mL)2 mL has grown after 6 hours,add hUCMSC(1 × 106/mL)2 mL as the experimental group,add equal amounts of phosphate buffer (PBS)for infection,A549 and PBS and the medium has grown as the control group. A549 cells morphological changes between the compared groups(Transmission electron microscope,TEM),A549 cell viability(new CCK-8 cell proliferation assay Kit),A549 cells apoptosis(Annexin V-FITC/PI double staining flow cytometry)and the expression of A549 pulmonary surfactant A(SP-A) (Western blot).[Results]Transmission electron microscope cell morphology observation displayed ,infection group A549 cell dam?aged obviously,cell quality appeared empty bubble degeneration,chromatin height agglutination,visible apoptosis bodies;experi?ment group cell package film structure full,nuclear film full,nucleolus obviously,nuclear chromatin electronic density low,chroma? tin uniform,no apoptotic bodies;control group A549 cell structure full,membrane surface micro-fluff rich,nuclear film full,nucle?ar week clearance structure normal,chromatin uniform;infection group and control group compared,Infection group A549 cell sur?vival significantly reduced[(70.35±2.89)% and(97.37±2.07)%,n=3,P<0.01],apoptosis rate significantly increased[(8.63%± 0.16)%and(2.55±0.11)%,n=3,P<0.01],In the infected group,PA could damage A549 cells and decrease the amount of SP-A ex?pression(n=5,P<0.05). In the experiment group,the protective effect of hUCMSC on the A549 cells after infection may increase the expression of SP-A(n=5,P<0.05);[Conclusions]HUCMSC inhibits the infection of A549 cells apoptosis and protection of A549 cells secrete SP-A.

Objective To improve the success rate of crystal embedding of human (animal) pipeline cast specimens for long-term preservation and application of cast specimens better. Methods The selection of embedding mold, specimen fixation, adjustment of the proportion of glue, grinding and polishing were improved, and a crystal embedding model of a fetal lung duct cast specimen was made to explore and optimize the simple and efficient production process of a crystal-embedded human (animal) pipeline casting specimen. Results The crystal model produced after the improvement had great transparency, beautiful shape, no bubbles, and no mold branches broken. The distribution and running of the casted branches of the fetal lung of the crystal model could be observed clearly in the embedded middle fetal lung through any angle and orientation, which was consistent with the cast specimens before embedding, and had a strong sense of three-dimensional space. Conclusion The improved process is better for embedding human (animal) pipeline casting specimens, which is conducive to long-term preservation. It is better for clinical anatomy teaching and exhibition in life science museum.

Objective To explore the effect and the mechanism of vitamin D(Vit D) promotes proliferation and differentiation of mesenchymal stem cells (MSCs) through regulates extracts of plastrum testudinis (PTE).Methods Established the PGL3-Id1 promoter and transfered rat MSCs.PTE combined with 10-6,10-7,10-8mol/L Vit D respectively were acted on the transfected MSCs for 36 hours.The level of Id1 promoter were detected by luciferase activity measurement.1,3,30,100 pg/mL PTE combined with Vit D of 10-7 mol/L were acted on MSCs for 36 hours,3 days and 7 days,and the VDR expression were detected by RT-PCR test.Results PTE promoted the expression of Id1 in MSCs,the expression of Id1 was inhibited when PTE combined with Vit D (P ＜ 0.01),and it was significantly different among different dosis of Vit D(P ＜0.01).The expression of VDR was inhibited in different degree when PTE combined with Vit D for 36 hours,3 days and 7 days.PTE combed with large dose of Vit D for 36 hours had significant effect of inhibition,and the difference was statistically significant (P ＜ 0.05).The inhibiting effect was more obvious when PTE combined with large dose of Vit D for 3 days and 7 days.When different doses of PTE combined with Vit D for a same duration,the difference of VDR expression was statistically significant (P ＜ 0.05).Meanwhile,when same doses of PTE combined with Vit D for different durations,the difference of VDR expression at 7 days and 36 hours was statistically significant (P ＜ 0.05).Conclusion The proliferation of MSCs which promoted by PTE was inhibited by Vit D,and the nuclear receptor VDR may be one of the targets of drug action for PTE regulating proliferation and differentiation of MSCs.

Inflammatory diseases are common medical conditions seen in disorders of human immune system. There is a great demand for anti-inflammatory drugs. There are major inflammatory mediators in arachidonic acid metabolic network. Several enzymes in this network have been used as key targets for the development of anti-inflammatory drugs. However, specific single-target inhibitors can not sufficiently control the network balance and may cause side effects at the same time. Most inflammation induced diseases come from the complicated coupling of inflammatory cascades involving multiple targets. In order to treat these complicated diseases, drugs that can intervene multi-targets at the same time attracted much attention. The goal of this review is mainly focused on the key enzymes in arachidonic acid metabolic network, such as phospholipase A2, cyclooxygenase, 5-lipoxygenase and eukotriene A4 hydrolase. Advance in single target and multi-targe inhibitors is summarized.
Animals ; Anti-Inflammatory Agents ; therapeutic use ; Arachidonate 5-Lipoxygenase ; metabolism ; therapeutic use ; Arachidonic Acid ; metabolism ; Cyclooxygenase Inhibitors ; therapeutic use ; Drug Delivery Systems ; methods ; Epoxide Hydrolases ; antagonists & inhibitors ; metabolism ; therapeutic use ; Humans ; Inflammation ; drug therapy ; Lipoxygenase Inhibitors ; Metabolic Networks and Pathways ; drug effects ; Phospholipase A2 Inhibitors ; Phospholipases A2 ; metabolism ; therapeutic use ; Prostaglandin-Endoperoxide Synthases ; metabolism