To study the change of c-fos mRNA and protein in hippocampus of morphine addicted mice after injected with ribozyme specially cleaving per1 mRNA.

To elucidate the antileukemi effects of berbamine and the possible molecular mechanisms in vitro and in vivo, MTT method was used to examine the effect of berbamine on K562 cell growth. The apoptosis rate was measured by flow cytometry. The mRNA expression level of BCR/ABL gene (semiquantity value) was determined by RT-PCR and the BCR/ABL protein (P210) level was detected by Western blot. The K562-bearing mice were used to reveal the therapeutic effect in vivo. The results showed that a significant time- and concentration-dependent inhibition of cell growth was found in the cells treated with berbamine. After the cells were exposed to 8.0 microg/ml berbamine for 24, 48 and 72 hours, the percentage of growth inhibition of K562 cells progressively increased by (26.63 +/- 3.57)%, (61.84 +/- 4.74)%, (75.32 +/- 1.95)%, respectively (compared with control, P < 0.01). The IC(50) (72 hours) value was 5.227 +/- 1.307 microg/ml. The apoptosis rate of K562 cells treated with 8.0 microg/ml berbamine for 24 and 72 hours increased from (29.20 +/- 3.82)% to (61.77 +/- 4.35)% (P < 0.01). Berbamine down-regulated the expression levels of bcr/abl gene and P210 in K562 cells in a time- and concentration-dependent manner. The bcr/abl expression decreased from (1.38 +/- 0.02) to (0.97 +/- 0.01) after exposure of the cells to 8.0 microg/ml berbamine for 0 and 72 hours (P < 0.01). When the cells were treated with 4.0 - 16.0 microg/ml berbamine for 24 hours, the level of P210 decreased from (0.95 +/- 0.03) to (0.63 +/- 0.01) (P < 0.01). In vivo, after treatment for 4 weeks, the tumor weight of berbamine-treated group was also lower than that of untreated group [(1.46 +/- 0.43) g vs (2.90 +/- 0.94) g, P < 0.01] and the inhibition rate was 49.66%, moreover, berbamine down-regulated the expression level of bcr/abl gene of tumor cells. It is concluded that berbamine can obviously inhibit the cell proliferation and induce apoptosis in K562 cell lines in a time- and concentration-dependent manner in vitro. The mechanisms of berbamine-induced apoptosis may be involved in down-regulation of bcr/abl gene expression and P210 level. In vivo, berbamine can aslo display a better antileukemic effect and down-regulate expression of bcr/abl gene. Berbamine extracted from Chinese herb may be a promising candidate of new drug for clinical anticancer treatment, especially for bcr-abl(+) diseases.

The permeability of cell membrane was enhanced by exogenous SA in the culture of Taxus cuspidata. Nuclei condense and fragments were observed in some cells by using fluorescent microscope, and the degraded chromosomal DNA was observed by using agarose gel electrophoresis. The changes in soluble proteins of the suspension cultures of Taxus cuspidata induced by salicylic acids were analyzed by using two-dimensional polyacrylamide gel electrophoresis. Comparing with the control, seven new protein spots were found and six protein spots were not found in the cultures grown with SA at 48h. The results obtained showed that SA could induce the expression of some special proteins that might be related with the action of SA in the suspension cultures of Taxus cuspidata.

Two different calmodulin-binding protein kinase cDNAs (NtCBK1/2) have been isolated from tobacco. To understand the CBK protein activity regulation, we compared the activity regulation of NtCBK1 and NtCBK2 by pH, Mg(2+) concentration and Na(+) concentration. We found the autophosphorylation of NtCBK1/2 reached the maximum in pH 7.5 and 8 respectively; Mg(2+) and Na(+) shown different effects on the activity of NtCBKs, high and low Mg(2+) concentrations both inhibited the activity of NtCBKs, but Na+ had little effect on the kinase activity. In addition, to obtain further insight about the physiological roles of individual NtCBKs, we detected the expression profiles of CBKs. The results revealed different patterns of expression of NtCBK1 and NtCBK2. Both are largely expressed in leaf and flower; but in stem and root, NtCBK1 gene had stronger expression than NtCBK2. NtCBK2 expression was induced by GA treatment, while NtCBK1 expression remained unchanged under GA treatment. Expression of both NtCBK1 and NtCBK2 increased in response to salt stress, the former to a greater extent, and both expressions did not change under high/low temperature, drought, NAA and ABA treatments.

To study the regulation of chromium on gene expression related to metabolism of skeletal muscles in diabetic rats.

To investigate the effects of interleukin 7 (IL-7) on B7 molecules expression and immunogenicity of acute leukemia (AL) cells.

To explore the effect of sodium butyrate (SB) on the expression of costimulatory molecules in acute leukemia cells and its mechanism.

To investigate the effect of arsenic trioxide on multiple myeloma (MM) cell gene expression and explore the molecular mechanism of arsenic trioxide therapy for MM.

To explore the effect of 2-methoxyestradiol (2ME2) and arsenic trioxide (As2O3) on the apoptosis related gene expression in multiple myeloma cell line CZ-1.

To study the effects of c9,t11-conjugated linoleic acid (c9,t11-CLA) on critical enzymes of linoleic acid metabolism in stomach granular cell (SGC-7901).

To investigate the role of matrix metalloproteinases (MMPs) in onset of labor, and the mechanism of diazepam in promoting cervical ripening.

To explore the inhibitory mechanism of phosphodiesterase(PDE) inhibitor on expression of IL-8 mRNA in peripheral blood mononuclear cells (PBMCs) from chronic obstructive pulmonary disease(COPD) patients.

To observe the synergistic role between rhIL-2 and adriamycin long circulating temperature-sensitive liposome (ALTSL) in targeting therapy of H22 tumor-bearing mice and explore their anti-tumor mechanism.

To investigate the regulation of soluble and membrane bound TNF-related apoptosis-inducing ligand (TRAIL) in Jurkt cells by phorbol myristic acctate (PMA), and the cytotoxicity of the two forms of TRAIL.

To explore the regulative action of IEGs when the nicotinic acetylcholine receptors (nAChRs) of PC12 cells were activated by anatoxin-a.

To control the expression of AAV-mediated glial cell-line derived neurotrophic factor (GDNF) gene purposely by incorporating novel Tet-On trans-activator rtTA2s-S2, which prevents potential harms caused by over-expression of recombinant target genes.

To investigate the effect of interferon-gamma (IFN-gamma) on airway mucous cells and its mechanisms.

To explore the sensitivity of survivin-positive primary acute leukemia (AL) cells to various chemotherapeutics, RT-PCR was used to detect the expression of survivin mRNA in AL cells, the cytotoxicity of chemotherapeutics was investigated with the MTT assay. The results indicated that for the primary AL cells cultured with various chemotherapeutics for 15 hours, the cytotoxicities of daunorubicin (DNR), homoharringtonine (HHT), aclacinomycin (Acla), Ara C (cytosine arabinoside), HA (HHT + Ara C), DA (DNR+Ara C) to the survivin-positive AL cells were similar with that to the survivin-negative AL cells. When AL cells were treated with AA (Acla + Ara C) in vitro, the cytotoxicity in survivin-positive group was apparently higher than that in survivin-negative group [(37.24 +/- 18.36)% vs (24.32 +/- 9.33)%, P = 0.032]. It is suggested that the survivin-positive AL cells may be sensitive to some chemotherapy, such as AA (Acla + Ara C).

To study the methylation in the promoter of LRP15 gene and its relationship with gene expression and to explore the possible mechanism of regulating LRP15 gene methylation, the methylation in the promoter of LRP15 gene in K562 cell line was detected by MS-PCR. Then K562 was exposed to 5-aza-2'-deoxycytidine (CdR) and trichostatin (TSA), to determine whether the silencing of LRP15 gene by de novo methylation could be reversed. As a result, it was confirmed by MS-PCR that the promoter of LRP15 was hypermathylated in K562 cell line, and lost its transcription activity. After CdR, with or without TSA, the silencing of LRP15 gene by de novo methylation can be reversed. Observation demonstrated that the expression of LRP15 was controlled by methylation in its promoter in K562. It is suggested that methyltransferase inhibitor and deacetylase inhibitor may be effective agents in leukemia therapy.

To investigate the effect of interleukin-10 (IL-10) on the expression of transforming growth factor-beta(1) (TGFbeta(1)) and platelet-derived growth factor (PDGF) in hepatic stellate cells (HSC) during liver injury.