The role of ADIPOQ methylation in curcumin-administrated experimental nonalcoholic fatty liver disease.

Objective: To investigate the role of adiponectin precursor (ADIPOQ) DNA methylation in the pathogenesis of nonalcoholic fatty liver disease (NAFLD) and the effect of curcumin on the development of NAFLD using rat models.

Methods: Male Sprague-Dawley rats were divided into the control, NAFLD and curcumin-treated groups. The genetic and epigenetic features of each rat were measured and recorded.

Novel syngeneic liver hapten protein compounds play different roles in pathogenesis of autoimmune hepatitis in the C57BL/6 mouse.

Background/aims: The autoimmune hepatitis (AIH) model in C57BL/6 mice with syngeneic hapten S100 and adjuvant injected intraperitoneally has been designed to elucidate the pathogenesis of AIH. Three separate hapten peak proteins, peak I, peak II and peak III, could be derived from S100, but little is understood their roles on the development of AIH. This study aims to learn more about these roles on pathogenesis of AIH.

Reversal of multidrug resistance by magnetic Fe3O4 nanoparticle copolymerizating daunorubicin and MDR1 shRNA expression vector in leukemia cells.

In many instances, multidrug resistance (MDR) is mediated by increasing the expression at the cell surface of the MDR1 gene product, P-glycoprotein (P-gp), a 170-kD energy-dependent efflux pump. The aim of this study was to investigate the potential benefit of combination therapy with magnetic Fe(3)O(4) nanoparticle [MNP (Fe(3)O(4))] and MDR1 shRNA expression vector in K562/A02 cells. For stable reversal of "classical" MDR by short hairpin RNA (shRNA) aiming directly at the target sequence (3491-3509, 1539-1557, and 3103-3121 nucleotide) of MDR1 mRNA.

Promoter hypermethylation and histone hypoacetylation contribute to pancreatic-duodenal homeobox 1 silencing in gastric cancer.

Background And Aims: The expression of pancreatic-duodenal homeobox 1 (PDX1) in gastric cancer is aberrantly reduced. The aim of this study was to elucidate the regulation of DNA methylation and histone acetylation at the promoter for PDX1 silencing in gastric cancer.

Methods: PDX1 expression in response to demethylation and acetylation was detected in human gastric cancer cell lines by reverse transcription-polymerase chain reaction (PCR) and western blot.

Effects of magnetic nanoparticle of Fe3O4 on apoptosis induced by Gambogic acid in U937 leukemia cells.

This study was aimed to explore the potential therapy of Gambogic acid (GA) combined with magnetic nanoparticle of Fe3O4 (Fe3O4-MNP) on leukemia. The proliferation of U937 cells and the cytotoxicity were evaluated by MTT assay. Cell apoptosis was observed and analyzed by microscopy and flow cytometry respectively.

Daunorubicin-loaded magnetic nanoparticles of Fe3O4 overcome multidrug resistance and induce apoptosis of K562-n/VCR cells in vivo.

Multidrug resistance (MDR) is a major obstacle to cancer chemotherapy. We evaluated the effect of daunorubicin (DNR)-loaded magnetic nanoparticles of Fe3O4 (MNPs-Fe3O4) on K562-n/VCR cells in vivo. K562-n and its MDR counterpart K562-n/VCR cell were inoculated into nude mice subcutaneously.

[Reversal effect of Fe3O4-magnetic nanoparticles on multi-drug resistance of ovarian carcinoma cells and its correlation with apoptosis-associated genes].

Background And Objective: Resistance to cisplatin (DDP) remains a major obstacle for the successful treatment of ovarian cancer. This study was to determine the reversal effect of Fe3O4-magnetic nanoparticles (MNPs) on DDP-resistance of ovarian carcinoma cell line SKOV3/DDP, and to explore its correlation with apoptosis-associated genes.

Methods: SKOV3/DDP cells were divided into the DDP group, the Fe3O4-MNPs group, the combination (DDP plus Fe3O4-MNPs) group, and the control group.

Daunorubicin-loaded magnetic nanoparticles of Fe(3)O(4) greatly enhance the responses of multidrug-resistant K562 leukemic cells in a nude mouse xenograft model to chemotherapy.

Multidrug resistance (MDR) plays a major role in the failure of cancer chemotherapy. Since Fe(3)O(4)-magnetic nanoparticle loaded with daunorubicin (DNR) can overcome multidrug-resistance of K562 cells in vitro, the effect of Fe(3)O(4)-magnetic nanoparticle loaded with DNR on multidrug-resistant K562 cells was studied in vivo, the K562-n and its MDR counterpart K562-n/VCR cells were inoculated subcutaneously into both sides of the back of nude mice to establish a human leukemia xenograft model. The mice were randomly divided into group A receiving normal saline, group B receiving DNR, group C receiving Fe(3)O(4)-magnetic nanoparticle, group D receiving Fe(3)O(4)-magnetic nanoparticle loaded with DNR and group E receiving Fe(3)O(4)-magnetic nanoparticle containing DNR with a magnetic field built on the surface of the tumor tissue.

Reversal of multidrug resistance in xenograft nude-mice by magnetic Fe(3)O(4) nanoparticles combined with daunorubicin and 5-bromotetrandrine.

This study was aimed to investigate the reversal effect of 5-bromotetrandrine (5-BrTet) and magnetic nanoparticle of Fe(3)O(4) (Fe(3)O(4)-MNPs) combined with DNR in vivo. The xenograft leukemia model with stable multiple drug resistance in nude mice was established. The two sub-clones of K562 and K562/A02 cells were respectively inoculated subcutaneously into back of athymic nude mice (1 x 10(7) cells/each) to establish the leukemia xenograft models.

Effects of magnetic nanoparticle of fe(3)o(4) and 5-bromotetrandrine on apoptosis of K562/A02 leukemic cells induced by daunorubicin.

The aim of this study was to investigate the potential benefit of combination therapy with magnetic nanoparticle of Fe(3)O(4) and 5-Bromotetrandrine (5-BrTet) on chronic leukemia. The apoptosis was detected by flow cytometry (FCM), Wright staining and light microscope; the expressions of BAX and BCL-2 were measured by Western blot. The results showed that combination of daunorubicin (DNR) with either MNP (Fe(3)O(4)) or 5-BrTet exerted a potent cytotoxic effect on K562/A02 cells, while MNP (Fe(3)O(4)) and 5-BrTet co-treatment could synergistically enhance DNR-induced apoptosis.