Cystic echinococcosis (CE) is a zoonotic infection caused by Echinococcus granulosus larvae. It seriously affects the development of animal husbandry and endangers human health. Due to a poor understanding of the cystic fluid formation pathway, there is currently a lack of innovative methods for the prevention and treatment of CE. In this study, the protoscoleces (PSCs) in the encystation process were analyzed by high-throughput RNA sequencing. A total of 32,401 transcripts and 14,903 cDNAs revealed numbers of new genes and transcripts, stage-specific genes, and differently expressed genes. Genes encoding proteins involved in signaling pathways, such as putative G-protein coupled receptor, tyrosine kinases, and serine/threonine protein kinase, were predominantly up-regulated during the encystation process. Antioxidant enzymes included cytochrome c oxidase, thioredoxin glutathione, and glutathione peroxidase were a high expression level. Intriguingly, KEGG enrichment suggested that differentially up-regulated genes involved in the vasopressin-regulated water reabsorption metabolic pathway may play important roles in the transport of proteins, carbohydrates, and other substances. These results provide valuable information on the mechanism of cystic fluid production during the encystation process, and provide a basis for further studies on the molecular mechanisms of growth and development of PSCs.

Objective To study the protection of L-ascorbic acid on mouse embryonic fibroblasts(NIH/ 3T3) from carcinogenic effects caused by nickel smelting smoke subjects.Methods The NIH/3T3 cells were divided into experimental and L-ascorbic acid in the intervention group.Plus exposure group concentration of nickel refining dusts were formulate 0.00,25.00,50.00,100.00 μg/ml suspension,the intervention group on the basis of the added exposure group containing L-ascorbic acid (100 mmol/L),contacted.Then,the cell viability was detected by MTT assay,we used Calcein-AM fluorescence probe to detect cell mitochondrial permeability transition pore (MPTP) changes,JC-1 staining to observe and detect the cell mitochondrial membrane potential (MMP) change,colorimetric quantitative to study the activity of mitochondrial respiratory chain complex Ⅰ,l,Ⅲ,Ⅳ.Results Upon 24 h incubation,both cell relative inhibition rate,openness of MPTP were increasing enhanced by different concentrations,on the other hand,MMP and the activity of mitochondrial respiratory chain complex Ⅰ,Ⅱ,Ⅳ were obviously decreased,the differences were statistically significant (P＜0.05).After L-ascorbic acid intervention treatment,the results of the intervention group were lower than that of the exposure group,and the difference was statistically significant (P＜0.05),indicating the protection of L-ascorbic acid on cell mitochondrial from the nickel exposure damage.Conclusion The damage effects of nickel on NIH/3T3 cell mitochondrial was significantly enhanced with the increasing concentration,and L-ascorbic acid has certain protection on cellular mitochondrial.

Objective To study the protection of L-ascorbic acid on mouse embryonic fibroblasts(NIH/ 3T3) from carcinogenic effects caused by nickel smelting smoke subjects.Methods The NIH/3T3 cells were divided into experimental and L-ascorbic acid in the intervention group.Plus exposure group concentration of nickel refining dusts were formulate 0.00,25.00,50.00,100.00 μg/ml suspension,the intervention group on the basis of the added exposure group containing L-ascorbic acid (100 mmol/L),contacted.Then,the cell viability was detected by MTT assay,we used Calcein-AM fluorescence probe to detect cell mitochondrial permeability transition pore (MPTP) changes,JC-1 staining to observe and detect the cell mitochondrial membrane potential (MMP) change,colorimetric quantitative to study the activity of mitochondrial respiratory chain complex Ⅰ,l,Ⅲ,Ⅳ.Results Upon 24 h incubation,both cell relative inhibition rate,openness of MPTP were increasing enhanced by different concentrations,on the other hand,MMP and the activity of mitochondrial respiratory chain complex Ⅰ,Ⅱ,Ⅳ were obviously decreased,the differences were statistically significant (P＜0.05).After L-ascorbic acid intervention treatment,the results of the intervention group were lower than that of the exposure group,and the difference was statistically significant (P＜0.05),indicating the protection of L-ascorbic acid on cell mitochondrial from the nickel exposure damage.Conclusion The damage effects of nickel on NIH/3T3 cell mitochondrial was significantly enhanced with the increasing concentration,and L-ascorbic acid has certain protection on cellular mitochondrial.