ABSTRACT
Objective::To finding the main research contents, research frontier, author and institutional cooperation of traditional Chinese medicine(TCM) for treating henoch-schonlein purpura(HSP). Providing reference for the research and development of TCM for treating the disease. Method::Using Citespace to analyze 2 878 TCM articles related to HSP retrieved from CNKI, cluster analysis and burst analysis of literature keywords, co-occurring authors and institutional cooperation analysis. Result::Since 1995, the number of related literature was growing rapidly and had been stable at more than 100 per year after 2005.Cluster analysis showed 32 clusters, consisting of 396 nodes and 638 lines. The main clustering results include Children with allergic purpura, blood-activating and stasis-resolving drug, Henoch-Schonlein purpura nephritis, blood-cooling drugs, clinical observation, etc. Break analysis yielded 52 emergent words. It can be seen that TCM treatment of HSP is mainly based on cooling blood, followed by activating blood to eliminate stagnation and clearing heat. Commonly used drugs are Moutan Cortex, Paeoniae Radix Rubra, and Rehmanniae Radix, etc. Clinically, it pays more attention to the experience of famous doctors, research on Children with allergic purpura, etc.The author's cooperation network has obtained the maps of the three main cooperation teams with DING Ying, SUN Yi-qiu and HE Ping as the core. The Density of institutional cooperation network is 0.007 1. Conclusion::The main research contents of TCM for treating HSP include Children with allergic purpura, blood-activating and stasis-resolving drug, HSP nephritis, blood-cooling drugs, clinical observation, etc. Children with allergic purpura, experience from famous doctor, HSP nephritis and clinical efficacy is the foremost current research hotspot. A number of research teams have been formed that are relatively stable, but the institutional cooperation is scattered.
ABSTRACT
To observe the contribution of FoxO1 on its downstream molecules expression and function in Jurkat cells,Jurkat cells were infected with FoxO1 expression lentivirus and interference lentivirus to establish FoxO1-KLF2-S1P1 signaling pathways mod-el.After infection of 120 h,FoxO1,KLF2,S1P1 and CD62L mRNA levels and the protein expression of FoxO1,FoxO1-p and KLF2 were increased (P<0.05) in FoxO1-overexpression group.Converse results(P<0.05) were observed in the interference group.The proportions of S1P1+cells were increased in both groups.It was notably that S1P1+cells were decreased(P<0.05) in interference group after infection of 72 h.The proportion of CD62L+cells was increased(P<0.05) in overexpression group,it was decreased(P<0.05) in the interference group.This vitro experiments showed S1P1 and CD62L could be regulated by FoxO1 lentivirus,and provided an experimental basis for research about intracellular FoxO1-KLF2-S1P1 signaling pathways and cellular functions.
ABSTRACT
This study was aimed to investigate the changes of differentiation and gene expression of CD133(+) cells in human umbilical cord blood induced by stem cell factor (SCF) and basic fibroblast growth factor (bFGF) in vitro, and to explore the biological characteristics of CD133(+) cells so as to provide experimental basis for potential use in regenerative medicine. The human umbilical cord blood CD133(+) cells were isolated from umbilical cord blood and purified by MACS magnetic selection. The CD133(+) cells were cultured in DMEM/F12 medium containing SCF, bFGF and B27 for 10 to 15 days. The total RNA of these cells was extracted before and after culture, and the analysis of related gene expression levels of these cells was performed using oligonucleotide microarrays. The results showed that out of 263 genes 21 genes were obviously up-regulated after culture than that before culture, whereas 7 genes were found to be significant down-regulated as compared with fresh-separated CD133(+) cells. These genes were involved in stem cell specific markers, cell cycle regulators, stem cell differentiation markers and signaling pathways that are important for stem cell maintenance. It is concluded that SCF and bFGF can induce differentiation of human cord blood CD133(+) cells through up- or down-regulation of specific genes. This study provides gene expression information for SCF and bFGF-induced human cord blood CD133(+) cells and contributes to understand the effect of SCF and bFGF on proliferation and differentiation CD133(+) cells at gene level, and promotes therapeutic applications of the CD133(+) cells induced by SCF and bFGF.