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[Objective]To review the antitumor progress of Raddeanin A in nearly 10 years. [Method] Col ecting the antitumor research literature about Raddeanin A for nearly 10 years, describing its antitumor research mechanism, such as inducting of cellapoptosis blocking the cellcycle, blocking STATs signaling pathways and inhibiting the tumor angiogenesis. [Result] Raddeanin A could induce the H460 cellapoptosis, block LoVo cellcycle and STATs signaling pathways of LoVo cells, and inhibit HepG-2 cellangiogenesis. [Conclusion] The antitumor mechanism of Raddeanin A could be inducting of cellapoptosis, blocking the cellcycle, blocking STATs signaling pathways and inhibiting the tumor angiogenesis.
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KLF9(Kruppel-likefactor9)isthetranscriptionfactorthatcanbindGC-richsitesthrough three C2H2-type zinc fingers and can regulate diverse biological processes,including cell proliferation,apopto-sis and the development of the organ.KLF9 is downregulated in some tumor specimens and tumorous cell lines relative to the normal samples and cell lines and plays an important role in the growth of cancer cells.Similar with the other KLF numbers,KLF9 could affect the development of tumors,especially for the endocrine-related cancers through multiple signaling pathways and interventions with other proteins.
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Objective ToexploreamethodofusingCaspase-3smallinterferenceribonucleicacid (siRNA)in vitro to decrease the apoptosis in stable cell lines of bone marrow mesenchymal stem cell (MSC)in ordertoestablishMSCcelllineswithstableexpression.Methods VirusparticlescontainingCaspase-3siRNA were generated in 293FT cells by retroviral packaging system,then were transfected into MSC of rats. And the transfected cells were screened and cultured to get the stable MSC lines. According to the characteristics of retrovirus,the stable expression of the cell lines was identified by Western blot and real-time fluorescent quantitative PCR (RT-QPCR). The apoptosis of stable cell lines and normal MSC were detected by terminal dexynucleotidyl transferase-mediated dUTP-biotin nick end labeling (TUNEL ) and their differences were compared.Results Comparedwiththenormalcells,thecaspase-3proteinexpressionandmRNAcontentof stable MSC lines were significantly reduced. In the same condition in vitro,the apoptosis quantity of stable MSC linessignificantlydecreasedcomparedwiththenormalcells.Conclusions StablecelllinesofMSCwithstable expression of Caspase-3 siRNA can be obtained by retroviral packaging system. The apoptosis quantity of stable MSC Lines significantly decreased compared with the normal cells.
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Objective To investigate the protective effects of bone marrow mesenchymal stem cells transplantation (MSCT) and mobilization on severe acute pancreatitis (SAP) with acute renal injury.Methods A total of 240 SD rats were randomly divided into sham operation group ( n =48 ),model control group ( n =48 ),MSCT group ( n =48),bone marrow mesenchymal stem cells mobilization (MSCM) group ( n =48) and MSCT +MSCM group ( n =48 ) according to the random number table.Rat models of SAP were made by peritoneal injection of L-arginine.Rats in the MSCT group were injected with 1.2 ml of bone marrow mesenchymai stem cells via femoral vein at 6 hours after SAP model establishment; rats in the MSCM group were subcutaneously injected with 40 μg/kg of granulocyte-colony stimulating factor (G-CSF) at 3 days before SAP model establishment; rats in the MSCT + MSCM group were injected with 1.2 ml of MSC and 40 μg/kg of G-CSF simultaneously; rats in the sham operation group were injected with equal volume of normal saline.According to different time points after operation,rats in each group were subdivided into 12 h,24 h,48 h and 72 h groups (n =12).At each time points after operation,the mortality rate,pathological changes of renal tissue,expression of Bax protein,Bcl-2 protein and apoptosis indexes of renal tubular epithelium cells were observed.The contents of tumor necrotic factor-α (TNF-α),interleukin-6 (IL-6),blood urea nitrogen (BUN),creatinine (Cr),lactate dehydrogenase (LDH) and C-reactive protein (CRP) were determined.All data were analyzed by using SNK-q test,Fisher exact probability and analysis of variance.Results All rats in the sham operation group were survived.The numbers of rats in the model control group survived at postoperative 48 hours and 72 hours were 11 and 8,respectively.No rat died at postoperative 48 hours in the MSCT group,MSCM group and MSCT + MSCM group.The numbers of rats survived at postoperative 72 hours in the MSCT group,MSCM group and MSCT + MSCM group were 11,10 and 11,which were not significantly different from the number of survived rats in the model control group (P ＞0.05).The pathological injuries of renal tissues were relieved in the MSCT group,MSCM group and MSCT + MSCM group when compared with model control group.The expression of Bax protein,Bc1-2 protein,renal tubular epithelium cell apoptosis indexes at 12-72 hours were 12.80 + 1.78-20.30 + 2.40,4.34 + 1.20-3.03 ± 1.06,12.65％ ±2.31％-35.10％ ± 5.54％ in the model control group,9.68 ± 2.11-17.01 ± 2.54,5.57 ± 1.35-4.13 + 1.05,6.20％ ± 1.53％- 17.50％ ± 2.80％ in the MSCT group,10.05 ± 2.17-16.81 ± 2.55,5.49 ± 1.48-4.19 ±1.05,6.41％± 1.64％-17.14％±2.27％ in the MSCM group,8.33 ±2.06-14.03 ±2.27,6.60 ±2.11-5.63 ±1.52,5.80％ ± 1.52％-12.30％ ±2.43％ in the MSCT + MSCT group.There were significant differences in the expressions of Bax protein at 24 and 72 hours,Bcl-2 protein at 48 and 72 hours,renal tubular epithelium cell apoptosis index at 24,48 and 72 hours between the MSCT group,MSCM group and MSCT + MSCM group ( P ＜0.05 ),but no significant difference was found between the MSCT group and the MSCM group ( P ＞ 0.05 ).The contents of TNF-α,IL-6,BUN,Cr,LDH,CRP in the MSCT group,MSCM group and MSCT + MSCM group were decreased when compared with those in the model control group,and a significant decrease of the 6 factors was observed in the MSCT + MSCM group.There were significant difference in the content of TNF-α at 72 hours,IL-6,BUN and Cr at 48 and 72 hours,LDH at 24,48 and 72 hours and CRP at 72 hours between the MSCT group,MSCM group and MSCT + MSCM group (P ＜0.05),while no significant difference was observed between the MSCT group and the MSCM group (P ＞ 0.05).Conclusion MSCT and MSCM can significantly protect acute renal injury in the progress of SAP,the probable mechanisms are pathological regeneration,anti-inflammatory effect and apoptosis inhibition of mesenchymal stem cells.
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Objective: To study the mechanism of K562 leukemia cells proliferation and apoptosis induced by emodin. Methods: Inhibitory effect of emodin on proliferation of K562 leukemia cells was assayed by MTT method. The morphologic changes of K562 cells were observed under microscop after Wight-Giemsa staining. Apoptosis was checked by Annexin V/PI. The changes of cell cycle and apoptosis were detected by flow cytometry. The activities of Caspase-3,8,9 were checked by chromatometry to analyze the apoptosis of K562 cells. Results: The proliferation of K562 leukemia cells was significantly inhibited by emodin. The IC50 of K562 cells inhibited with emodin for 24 h,48 h and 72 h were 80,50 and 40 ?mol/L respectively. Typical morphological changes of K562 cells were observed by microscopy. The proliferation of K562 cells was obviously inhibited in dose-dependent manner. In Annexin V/PI,emodin induced K562 cells toward apoptosis in dose-dependent manner(P
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Objective To study clusterin expression in bladder cancer cell line EJ and its antiapoptosis mechanism. Methods The expression of clusterin in EJ cells was detected by means of immunocytochemical staining and its effect on apoptosis studied by 3′TUNEL method. Results Clusterin expressed clearly in EJ cells.Likewise,when a small dose of clusterin was added,clusterin was stained strongly in the cytoplasm of the EJ cells and MMC induced apoptosis of the EJ cells was markedly inhibited. Conclusions Clusterin can penetrate the cell membrane getting into the cell cytoplasm and there in the cytoplasm the antiapoptosis effect is evoked.By detecting the clusterin expression,recurrence and multidrug resistance of a bladder cancer may be evaluated.It is hopeful that the use of clusterin antibody in the treatment of bladder cancer might be feasible.