Inflammatory priming adipose derived stem cells significantly inhibit the proliferation of peripheral blood mononuclear cells / 北京大学学报(医学版)

OBJECTIVE@#To explored whether adipose derived stem cells (ASCs) could inhibit the pro-liferation of peripheral blood mononuclear cells (PBMCs) and whether inflammatory priming could enhance this property of ASCs.@*METHODS@#We isolated ASCs using collagenase from adipose tissue and expanded them in vitro. Cells were induced to differentiate into adipogenic and osteogenic lineages. The cells at passage 3 to passage 5 were used for the experiments. After carboxy fluoresce in succinimidyl ester (CFSE) staining, PBMCs were co-cultured with inflammatory priming ASCs. The PBMCs cultured without ASCs or with non-treated ASCs defined as control groups. Then we used flow cytometry to detect the proliferation of PBMCs.@*RESULTS@#ASCs had fibroblast-like phenotype and were spindle shaped. They were able to differentiate into cells of adipogenic and osteogenic lineages in specific induction media. ASCs had the CD expression profile consistant with the International Federation for Adipose Therapeutics statement. The percentage of parent cells in PBMC after co-cultured with ASCs increased, though there was no statistical significance. However, when co-cultured with inflammatory priming ASCs, the percentage of parent cells significantly increased (with inflammatory priming ASCs group vs. without ASCs group, 38.7%±10.0% vs. 28.4%±8.9%, P<0.05). This indicated that inflammatory priming ASCs could significantly inhibit the proliferation of PBMCs.@*CONCLUSION@#Inflammatory cytokines can enhance the immunosuppressive ability of ASCs. Our findings may help the application of ASCs in tissue repairment with better results.

Identification of molecular mechanism of necroptosis mediated by PI3K / 军事医学

Objective To identify the molecular mechanism of phosphatidylinositol-3-kinase (PI3K) in mediating necroptosis induced by tumor necrosis factor alpha (TNFα).Methods RNA interference mediated by lentivirus short hairpin RNA(shRNA) was used to downregulate p110α in L929 cells and Western blotting was used to determine the knockdown efficiency.In addition,Western blotting was used to detect the phosphorylation level of RIP1,RIP3 and MLKL in L929 cells treated with or without TNFα plus Z-VAD.Duolink assay kit was used to detect the interactions between different proteins or the same proteins.Results p110α knockdown was efficiently mediated by the lentivirus shRNA,which significantly suppressed the phosphorylation of RIP1,RIP3 and MLKL in the absence or presence of TNFα plus Z-VAD stimulation.Moreover,the interactions between p110α and RIP3,but not RIP1,increased in a time-dependent manner during the process of necroptosis,and p110α knockdown significantly inhibited the formation of necrosome and RIP1 homodimer or RIP3 homodimer.Conclusion PI3K mediates the TNFα-induced necroptosis by promoting the activation of RIP1/RIP3/MLKL signaling pathway.Given the increasing direct interactions between p110α and RIP3 during the process of necrosome formation,PI3K may regulate RIP3 kinase activity via direct phosphorylation of RIP3.

Protective effect of salidroside on contrast-induced nephropathy in comparison with N-acetylcysteine and its underlying mechanism / 中国结合医学杂志

<p><b>OBJECTIVE</b>To study the prevention effect of salidroside on contrast-induced-nephropathy (CIN) and its underlying mechanism.</p><p><b>METHODS</b>A total of 24 Wistar rats were randomly divided into 4 groups with 6 in each group. Rats were firstly administrated with normal saline (control and model groups), N-acetylcysteine (NAC, NAC group) and salidroside (salidroside group) for 7 days before model establishment in each group, respectively. Histopathological analysis was performed by periodic acid-Schiff (PAS) staining. Oxidative stress related parameters including superoxide dismutase (SOD) and methane dicarboxylic aldehyde (MDA), nitric oxide (NO), angiotensin II (Ang II), 8-hydroxy-2'-deoxyguanosine (8-OHdG), mRNA and protein levels of endothelial nitric oxide synthase (eNOS), and nitric oxide synthase (NOS) activity were measured.</p><p><b>RESULTS</b>Compared with the control group, the levels of MDA, Ang II and 8-OHdG were all significantly increased and levels of SOD, NO, and eNOS mRNA and protein were decreased significantly in the model group (P<0.05). Meanwhile, the NOS activity was also significantly decreased in the model group (P<0.05). In addition, the levels of these parameters were all improved in the NAC (P<0.05) and salidroside groups and no significant different was found between these two groups (P>0.05).</p><p><b>CONCLUSION</b>Salidroside can be the potential substitute of NAC to prevent CIN. The underlying mechanism may be associated with oxidative stress damage caused by contrast agents.</p>

Analysis on processing mechanism of calamine / 中国中药杂志

<p><b>OBJECTIVE</b>To study processing method and mechanism of Calamine.</p><p><b>METHOD</b>Thermogravimetry analysis method and nano-technology were adopted to analyze and synthesize the components in Calamine, Tetracycline was took as the comparison drug to determine the antibacterial activity of Calamine and its components.</p><p><b>RESULT</b>A part of zinc carbonate in Calamine was decomposed into zinc oxide when processing, and the particle size was smaller than before. The antibacterial activity of Calamine is decided by the content and particle size of zinc oxide, and has nothing with zinc carbonate. The more content and the smaller particle size of zinc oxide, the more powerful antibacterial activity of Calamine.</p><p><b>CONCLUSION</b>The content and the particle size of zinc oxide can be the important targets in the processing of Calamine.</p>