To observe the effect of IPS-B2 on mouse peritoneal macrophages and the transcription of IL-1beta, IL-6, TNF-alpha and iNOS.

To observe the effect of Bawei Xilei powder on CD3, CD4, CD8 T-lymphocytes in peripheral blood and colonic mucosa of rat with ulcerative colitis.

To explore the effect mechanism of Sanlengwan (SLW) on estrogen production in ectopic endometrium of rats.

Heme oxygenase-1 (HO-1) is a cellular stress protein, and its expression plays an important regulatory role in a lot of physiological and pathological processes. Although the expression of HO-1 in most tissues of body is low, a number of clinical and pharmacological experiments have proved that many compounds can induce HO-1 expression. The increase of HO-1 expression is the result of regulating different signaling pathways and transcription factors, and this induction of HO-1 is suggested to be partially therapeutic efficacy of these compounds. This article summarizes some kinds of compounds in this field of research at home and abroad over the last 10 years, and provides a brief analysis of the mechanism.

To evaluate the effect of mifepristone in reversing multidrug resistance(MDR) and modulating glucosylceramide synthase (GCS) mRNA expression in human ovarian cancer COC(1)/DDP cells.

To develop a tight tetracycline-controlled HCV-C double transgenic mouse model.

To investigate the effect of conjugated trienoic fatty acids on the growth inhibition, apoptosis in rat glioblastoma cells and to elucidate its mechanism of activity.

The full length cDNA of a novel metallothionein (LbMT2) gene was cloned from a cDNA library of Limonium bicolor. The LbMT2 gene cloned is 518 bp in length, which includes a 64 bp of 5' untranslated region (UTR) and a 205 bp of 3' untranslated region. This gene has an open reading frame (ORF) of 249 bp in length, encoding a protein of 82 amino acid residues with the molecular mass of 8.1 kDa and theoretical pI of 4.71. The expression of LbMT2 gene in L. bicolor in response to CuSO4, CdCl2, NaCl, cold, and PEG was further investigated using real time quantitative PCR. In both leaf and root of L. bicolor, the expression of LbMT2 was induced by CuSO4, CdCl2, NaCl, and cold, but inhibited by PEG stress. LbMT2 gene was inserted into a prokaryotic expression vector (pGEX-4T-2) to produce the recombinant expression vector pGEX-LbMT2. The expression of LbMT2 in E. coli BL21 was induced with IPTG, which produced a protein band with expected size of 35 kDa on SDS-PAGE.

A 1,700 bp DNA fragment, OsCDPK7 gene, was cloned with RT-PCR from liaoyan241 leaf treated under a low temperature of 4. Compared to the OsCDPK7 gene reported before (GenBank accession No. AB042550), this fragment, lack of 26 amino acids, possesses the activity of Ca2+-dependent protein kinase because of a complete integration of the Ca2+ binding structure domain and Ser/Thr protein kinase activity center. Plant expression vector was constructed,, OsCDPK7 gene was regulated by E12 promoter. OsCDPK7 gene was transferred into rice via Agrobacterium-mediated method. After Km screening and Southern blot, 10 transgenic plants were obtained. The analysis on the salt tolerance showed that the expression of OsCDPK7 gene composition enhanced the salt tolerance of T2 transgenic plants, part of T2 transgenic seeds could germinate in 0.2 mol/L NaCl medium, and T2 transgenic young plants could rejuvenate after treatment with 0.4 mol/L NaCl for 10 days, while the controlled plants could not germinate and died in salt stress. This research finding proved that the regulation factor of the plant signal transduction could enhance the salt tolerance of transgenic plants, while OsCDPK7 expression was different in the different tolerence transgenic plants.

Kosteletzkya virginica L. Presl. is an obligate wetland species indigenous to southeastern US. Its niche in salt marsh foretells its high salinity tolerance. cDNA-AFLP technique was used to identify the gene transcriptional profiles of leaves and roots from K. virginica seedlings under salt stress in order to clarify the molecular architecture of stress tolerance in the dicot halophyte. Expression analysis over time intervals and under various salt stresses in leaves or roots showed that the quantitatively expressed pattern (in which genes were quantitatively up- or down-regulated under salt stress or fluctuate with different NaCl concentrations) was more prevalent than the qualitatively expressed pattern (in which genes were induced or silenced under salt stress) in K. virginica seedlings under salt stress. The qualitative pattern was appreciably more predominant than the quantitative one only in roots when exposed to salt stress for 2 h. Although each expression pattern was observed in leaves as well as in roots, the percentage of genes (i.e., up-/down-regulated or induced/silenced under salt stress) was dynamically changeable under salt stress at different time intervals. All these results indicated that there was no established formula of gene expression patterns in deciphering the sophisticated mechanism of plant salinity tolerance, considering that plants undergo a series of dynamically physiological and metabolic pathways in sensing and response to salt stress for different tissues and during different stages of stress. A number of Trivially distributed file system (TDFs) up-regulated or induced under salt stress from leaves and roots were sequenced, and the sequences were blasted against the NCBI non-redundant protein database using translated nucleotide query (Blastx). The TDFs from K. virginica seedlings involved in sensing and response to salt stress can be classified at least into three groups according to their putative functions: (1) genes for re-establishing ionic homeostasis or preventing from damage (specially genes for transporter); (2) genes for resuming plant growth and development under salt stress, such as key enzymes involved in energy synthesis or hormone regulatory pathway; (3) genes for signal transduction and so on. The relationship of expression patterns of these TDFs with the molecular mechanism of salt tolerance in K. virginica was discussed.

To investigate effects of Sargassum confusum polysaccharide (SP) on the expressions of p53 and Rb genes.

This study was purposed to investigate the effects of angelicasinensis (Oliv) Diel compound injection, vauqueline, ephedrine and strychnine on human erythroleukemia multidrug resistance (MDR) K562/A02 cell line Mdr1 gene and p-glycoprotein. The MTT and trypan blue methods were used to analyze the cytotoxic effect of above-mentioned traditional Chinese drug; the expressions of K562/A02 cells Mdr1 gene and p-glycoprotein were detected by semi-quantitative reverse transcription polymerase chain reaction (RT-PCR) and Western blot respectively. The results showed that after K562/A02 cell were treated with angelicasinensis (Oliv) diels compound injection, vauqueline and ephedrine, mRNA transcription of Mdr1 gene was reduced significantly (p < 0.01); the expression of P-gp also decreased (p < 0.01). The expression level P-gp in group treated with vauqueline was the lowest, but the Mdr1 mRNA level and expression of P-gp of K562/A02 cells treated with strychnine did not obviously changed. It is concluded that angelicasinensis (Oliv) diels compound injection, vauqueline, ephedrine can partly reverse the multidrug resistance of K562/A02 cells, the down-regulation of Mdr1 gene causing decrease of p-glycoprotein expression may be one of the MDR reversal mechanisms in K562/A02 cells.

The aim of this study was to investigate the inhibitive effect of artesunate (ART) on CML cell line K562 and its influence on VEGF expression in vitro. Human CML cell line K562 cells were cultured in RPMI 1640 medium supplemented with 10% heat-inactivated fetal calf serum. All cells were cultured in a humidified atmosphere of 5% CO2 at 37.0 degrees C. K562 cells in logarithmic growth phase were collected and seeded in RPMI-1640 medium, and were treated with ART. At the indicated time points, viable cells were counted by trypan blue exclusion method. Each assay was triplicated. K562 cells were treated with ART at different concentrations. Morphological changes were observed with invert microscope. VEGF expression in K562 cells treated with ART at different concentrations and in the control group were detected by enzyme-linked immunosorbent assay (ELISA). The results indicated that ART obviously induced growth inhibition in K562 cells. The relationship between cell inhibition rates and the concentrations of ART showed a dose-dependent manner (p < 0.01). VEGF expression of K562 cells treated with ART at different concentrations decreased significantly (p < 0.01). No significant change of VEGF expression in control group was observed (p > 0.05), while VEGF expression was down-regulated significantly in experiment groups (p < 0.01). The inhibition rate of K562 cells increased in time and concentration-dependent manners. In K562 cell lines treated with ART, VEGF expression was up-regulated at first and then down-regulated to a lower level. It is concluded that ART inhibits k562 cell proliferation in a dose and time dependent manner. The mechanism underlying the inhibitive effect of ART on K562 cells may be realized through down-regulation of VEGF expression.

The purpose of this study was to investigate the effects of chloroquine diphosphate on the proliferation and apoptosis of human leukemic K562 cells, and to elucidate its possible mechanism of activity. The inhibitory effect of chloroquine diphosphate with different concentrations on K562 cell proliferation was detected by MTT method. Apoptosis was measured by flow cytometry (FCM); morphological analysis of apoptosis was performed after staining with propidium iodide (PI) under fluorescence microscope; cell apoptosis was assessed by the DNA ladder shown agarose gel electrophoresis. After treatment with chloroquine diphosphate, K562 cells were stained by Rhodamine 123 to detect changes in mitochondrial transmembrane potential (DeltaPsim) by FCM. The results showed that the cell viability decreased in dose-dependent manner, following chloroquine diphosphate treatment at different concentrations (1.5625, 3.125, 6.25, 12.5, 25, 50 and 100 micromol/L) for 24, 48 and 72 hours. By FCM analysis, the significant increases of sub-G(1) were observed. DNA ladder was detected and apoptotic nuclei were observed. DeltaPsim decreased in K562 cells after chloroquine diphosphate treatment. It is concluded that the chloroquine diphosphate can inhibit the proliferation of K562 cells and induce cell apoptosis, which may relate to down-regulation of mitochondrial transmembrane potential (DeltaPsim).

Geldanamycin (GA), an ansamycin antibiotic specifically binding heat shock protein 90 (Hsp90), exhibits a broad-spectrum antiviral effect. Herpes simplex virus type 1(HSV-1) replication in vitro was significantly inhibited by GA treatment. To explore the antiviral mechanism of GA against HSV-1, the 7267-spot human long oligonucleotide microarrays were applied to investigate the genes which might involved in the antiviral activity of GA in HeLa cells infected by HSV-1. Meanwhile, the reverse regulation of GA and HSV-1 on ACTG1, RAN, SOD1, HYAL1 were validated by using semi-quantitative RT-PCR. It is the first report of gene expression profile in cells infected by virus with GA treatment. The general impact of GA on cellular transcription may help to gain an insight into mechanism of its antiviral effect.

To study the influence of siRNA inhibition of CENP-A expression on the biological behavior of HepG2 cells.

To investigate the inhibitory effect on MTA1 gene by MTA1 short hairpin RNA (shRNA), downstream regulation of expression of ERa and invasion of human breast cancer cells.

The mechanisms by which emodin induces apoptosis and inhibits proliferation of cancer cells remain unclear. In this study, we investigated whether the proapoptotic effect of emodin on human NIH-H460 lung cancer cells and SMMC-7721 liver cancer cells was related to regulating RXR expression and function. MTT assay and DAPI staining were used to detect the anti-proliferative and apoptotic effects of emodin with or without 9-cis-retinoid acid on H460 and SMMC-7721. The reporter assay was used to detect the effect of emodin on RXR homo- and hetero-dimer transactivation. Competitive ligand binding assay was carried out to detect whether emodin could directly bind to RXR. The result showed that emodin could strongly inhibit the proliferation and induce apoptosis of both cancer cell lines, which could be antagonized by 9-cis-RA. The reporter assay showed that emodin could inhibit the transcriptional effect of the homo- and hetero-dimer transactivation of RXRalpha dose-dependently. However, in vitro binding assay did not show that emodin bind to RXRalpha-LBD directly. The findings suggest that exhibition of emodin its anti-cancer activity may be associated with involvement of RXRalpha signal transduction pathways.

To investigate the effect and mechanism of E-leng Capsule (ELC) in preventing and treating post-operation recurrence of ovarian endometriotic cysts (OEC).