Protective effect of raspberry extract on ConA-induced acute liver injuryin mice / 中国中药杂志

In this experiment,the antioxidant capacity of raspberry extract and the protective effect on liver injury induced by ConA in mice were investigated. Balb/C male mice were randomly divided into six groups: normal group,model group,bicyclol control group( 200 mg·kg~(-1)),low-dose raspberry extract group( 200 mg·kg~(-1)),middle-dose raspberry extract group( 400 mg·kg~(-1)),and highdose raspberry extract group( 800 mg·kg~(-1)). Each group was intragastrically administered with drugs according to the body weight once a day. Seven days later,all of the groups except for the normal group were treated with ConA( 20 mg·kg~(-1)) through tail vein injection to establish the acute liver injury model. The mice were put to death 8 hours later. The organ indexes were calculated. These rum levels of ALT,AST and LDH and the activities of SOD,CAT,GSH and MDA in liver tissue were detected. HE staining was used to observe the pathological changes of liver tissue in mice. Western blot was used to detect the expressions of Bax,Bcl-2,Nrf2 and Keap-1. The antioxidant capacity of raspberry extract was measured by CAA assay. The results showed that,raspberry extract had a strong antioxidant capacity. Simultaneously,compared with the model group,raspberry extract can significantly improve the pathological conditions of liver,and significantly reduce ALT,AST and LDH activities in serum of liver injury mice( P<0. 01). The activities of SOD,CAT in liver homogenate supernatant were significantly increased in the high-dose group,the content of GSH increased,while the content of MDA was sharply declined in the high-dose group( P<0. 01). Meanwhile,raspberry extract down-regulated the expressions of Bax and Keap-1 and up-regulated the expressions of Bcl-2 and Nrf2. CAA showed that the compound raspberry extract had a strong antioxidant capacity. Therefore,raspberry extract has an obvious protective effect on acute liver injury induced by ConA in mice.

Study on Flk1 Cells during Mouse Early Embryogenesis by Lineage Tracing / 中国实验血液学杂志

OBJECTIVE@#To understand the differentiation of mesoderm-derived Flk1 cells on different locations of the early mouse embryonic development and to explore the potential of Flk1 cells to differentiate into mesenchymal lineage, like pericytes during vascular development.@*METHODS@#Based on the Cre-LoxP system conditional knockout study strategy, the Flk1-Cre mice and ROSA26 reporter mice were used for lineage-tracing studies. The fate of the Flk1 progenitor cells was traced with the GFP population. The detection of mesoderm marker Flk1, hematopoietic cell-specific marker CD45, endothelial cell-specific markers CD31, CD144, and Emcn (endomucin), pericyte specific markers PDGFRβ and NG2, using the methods of immunohistochemistry, immunofluorescence, and flow cytometry should be combined to solve the concerned problems.@*RESULTS@#Immunohistochemical staining of different fractions of E8.5-10.5 in the early embryogenesis of Flk1-Cre; ROSA26-EYFP mouse lineage showed that there were multiple populations in the Flk1 cell-derived GFP population surrounding hematopoietic sites, such as dorsal aortas, limb buds and yolk sac. In addition to hematopoietic cells, the CD31/Emcn typical endothelial cells distributed specifically along the blood vessel wall, there were many types of cell populations, such as mesenchymal-like cells. The immunofluorescence demonstrated that the cells of this group are neither hematopoietic, non-endothelial cells around the blood vessels, which are NG2+ pericytes. FACS analysis also confirmed that Flk1 cells contributed to pericytes. In addition, in different hematopoietic sites of the embryo, a small population of CD31+CD140B+ cell populations with a mesenchymal-like morphology was observed in the GFP population.@*CONCLUSION@#In the early stages of embryogenesis, mesoderm-derived Flk1 populations not only contribute to hematopoietic, endothelial, and muscle lineages, but also have a differentiation potential for mesenchymal lineage, like pericytes. The presumably observed CD31CD140B cell population may be a group of endothelial cells differentiated from Flk1 progenitor cells and undergoing an endothelium-to-mesenchymal transition, EndMT, gradually losing the endothelial surface-specific marker and also starting to express a pericyte surface-specific marker.

Efficacy of Xuebijing for coagulopathy in patients with sepsis

To provide evidence of the clinical efficacy of Xuebijing [XBJ] on blood coagulation in patients with sepsis. We conducted this meta-analysis in The People's Hospital of Liaoning Province, Shenyang, China between December 2013 and May 2014. We searched a number of databases for relevant randomized controlled trials [RCTs] published before December 2013 using the keywords [Xuebijing], [coagulation] and [sepsis]. Statistical analysis was performed with Review Manager 5.2 from the Cochrane Collaboration. Fourteen RCTs involving 867 patients were included. Compared with placebo, XBJ injection significantly improved platelets [mean differences [MD] = 42.14, 95% confidence interval [CI]: 22.42 - 61.86, p<0.00001], shortened the activated partial thromboplastin time [MD = -4.81, 95% CI: -7.86 - [-1.76], p=0.002], shortened the prothrombin time [MD = -2.33, 95% CI: -4.15 - [-0.51], p=0.01], and shortened the thrombin time [MD = -2.05, 95% CI: -3.52 - [-0.58], p=0.006]. However, no significant difference was found between the XBJ injection and the placebo group for fibrinogen [MD = 0.21, 95% CI: -0.38 - 0.81, p=0.48]. Xuebijing injection may improve coagulopathy in patients with sepsis. High-quality and large sample clinical trials are needed for confirmation

Effect of bortezomib on sensitization of HL-60 cells to TRAIL / 中国实验血液学杂志

This study was aimed to explore whether bortezomib can sensitize HL-60 cells to TNF-related apoptosis-inducing ligand (TRAIL) and to investigate its possible mechanism. The HL-60 cells were treated by different concentrations of TRAIL combined with subtoxic concentration of bortezomib. The proliferative inhibition of treated HL-60 cell was analysed by MTT assay. The cell apoptosis was determined by flow cytometry with Annexin V/PI double staining and the expression of caspase-8 was detected by Western blot. The results showed that the subtoxic concentration of bortezomib combined with 10 ng/ml of TRAIL enhanced apoptosis of HL-60 cells, as compared with TRAIL used alone; the expression of caspase-8 increased correspondingly. It is concluded that subtoxic concentration of bortezomib can sensitize HL-60 cells to TRAIL and its mechanism may be related to upregulation of caspase-8 expression.