cAMP response element binding protein(CREB) is a genetranscription regulator locating in the nucleus.The activated CREB by phosphoration plays an important role by binding to the cAMP response elements and modulate the transcription of various target genes.In addition,the activity of CREB is also regulated by lots of transcriptional regulators in signal transduction mechanism.In central nerve system,CREB participates in promoting neuron growth,the processes of plasticity and long term memory.More importantly,researches of CREB in the pathological processes of Alzheimers disease,Hungtingtons disease and HIV-related dementia have made a progress recently,providing a basis for some therapy strategies to the related neurodegenerative disorders.

Objective: To observe the effects of Tenglong Buzhong Decoction (TLBZD), a compound traditional Chinese herbal medicine, on proliferation and apoptosis of colon carcinoma cell line LS174T in vitro. Methods: Human colon carcinoma cell line LS174T and human colon epithelial cell line CRL-1790 were treated with different doses of TLBZD. Cell proliferation was detected with cell counting kit-8 (CCK-8) assay and clone formation assay. Cell cycle and apoptosis were detected by flow cytometry, and caspase-3, -8 and -9 activities in LS174T cells were detected by colorimetric assay. Results: TLBZD had no obvious cytotoxicity in normal CRL-1790 cells. After 72-hour treatment of 1 mg/mL TLBZD, or 48- and 72-hour of 2 mg/mL TLBZD, or 24-, 48- and 72-hour of 5-20 mg/mL TLBZD, proliferation of LS174T cells was significantly inhibited. Clone formation of LS174T cells was significantly inhibited by 1 to 20 mg/mL TLBZD treatment. TLBZD at doses of 5 to 20 mg/mL also induced apoptosis and cell cycle arrest at G(0)/G(1) phase in LS174T cells. In addition, caspase-3, -8 and -9 activities were significantly elevated after 5 to 20 mg/mL TLBZD treatment. Conclusion: TLBZD can inhibit cell proliferation, arrest cell cycle at G(0)/G(1) phase, and induce apoptosis in LS174T cells, which may be related to activating of caspase-3, -8 and -9.

Cell senescence is an important anti-cancer mechanism and may contribute to cancer therapeutic outcome. The present study observed the effects of Tenglong Buzhong Decoction (TLBZD), a Chinese herbal formula, on senescence in human colon carcinoma LS-174-T cells.

Objective To construct the short hairpin RNA recombinant plasmids targeting mdr1 gene which expresses highly in ovarian cancer resistance strain SKOV3/TAXOL to silence endogenefic mdr1 gene expression and investigate the role of mdr1 gene in the development of resistant ovarian cancer. Methods The pGPU6/GFP/Neo-mdr1 were constructed by gene clone technology. The influence on proliferation and apoptosis were investigated by CCK-8 in SKOV3/TAXOL after transfected pGPU6/GFP/Neo-mdr1. Results The expression against mdr1 proteins were inhibited by pGPU6/GFP/Neo-mdr1. The cell proliferation were inhibited after transfected pGPU6/GFP/Neo-mdr1 by CCK-8. The apoptosis were observed in DAB experiments and the apoptosis rate increased. Conclusion mdr1 plays an important role in proliferation of resistant ovarian cancer and the short hairpin RNA of mdr1 can efficiently suppress mdr1 expression and enhance the apoptosis in SKOV3/ATAXOL.

Objective To research the action mechanism of Chinese FormulaXuetongling on MDA-MB-231 human breast cancer cell invasion.Methods Transwell Invasion assay was applied to investigate the inhibitory effects on cancer cell invasion ofXuetongling extract in different concentrations;MMP-9 secretion activity was detected by zymography assay after the treatment of XTL extract in MDA-MB-231;Western blot was used to detect the effect of XTL extract on MMP-9 protein expression in MDA-MB-231.ResultsXuetongling extract in different concentrations significantly suppressed the cell invasion, MMP-9 secretion and MMP-9 protein expression in dose dependent manner.Conclusion The inhibitory effect ofXuetongling on MDA-MB-231 cell invasion may be due to the down-regulation of both MMP-9 secretion and MMP-9 protein expression.

Objective To explore the improvement effect of humanistic care on cognitive function impairment and living ability of patients with Alzheimer's disease. Methods 76 patients with Alzheimer's disease from January 2009 to May 2011 were taken as the research object.They were randomly divided into the control group and the observation group with 38 cases in each group.The control group was given conventional procedures for nursing care,and the observation group used humanistic nursing care as the guidance.The MMSE scale score,living ability index and family satisfaction degree before nursing and 1 month and 3 months after nursing for the two groups were taken for statistical comparison. Results The proportion of patients whose MMSE scale≥ 21 points and living ability score ranging from71 to 95 1 month and 3 months after care were higher than those of the control group.The satisfaction degree of patients in the observation group was also higher than the control group. Conclusions Humanistic care can significantly improve the cognitive dysfunction and living ability of patients with Alzheimer's disease,besides,family members of patients are more satisfied with this nursing model.

Objective To construct the small hairpinRNA recombinant plasmids targeting mdr-1 gene which expresses highly in ovarian cancer resistance strain SKOV3/TAXOL to silence endogenetic mdr-1 gene expression and investigate the role of mdr-1 gene in the development of resistant ovarian cancer. Methods The pPGPU6/GFP/Neo-mdr-1 were constructed by gene clone technology. The influence on proliferation and apoptosis were investigated by CCK-8 in SKOV3/TAXOL after transfected. pPGPU6/GFP/Neo-mdr-1. Results The expression against mdr-1 proteins were inhibited by pPGPU6/GFP/Neo-mdr-1. The cell proliferation were inhibited after transfected pPGPU6/GFP/Neo-mdr-1 by CCK-8. The apoptosis were observed in DAB experiments and the apoptosis rate incised. Conclusion mdr-1 plays an important role in proliferation of resistant ovarian cancer and the short hairpinRNA of mdr-1 can efficiently suppress mdr-1expression and enhance the apoptosis in SKOV3/TAXOL, which provides a novel method for chemotherapy resistant tumors.

Objective To explore whether pioglitazone can ameliorate radiation-induced fibrosis in rat heart.Methods A total of 46 Sprague-Dawley rats were divided into six groups (control group, pioglitazone (Pio) 10 mg·kg-1 ·d-1 group, Pio 20 mg·kg-1 ·d-1 group, 18 Gy irradiation + placebo group;18 Gy irradiation + Pio 10 mg·kg-1 ·d-1 , and 18 Gy irradiation + Pio 20 mg·kg-1 ·d-1 group).Experimental animals were exposed to radiation at the chest, then administered Pio or placebo for one month.At 3 months later, the rats were killed and their heart tissues were collected for Masson staining, Western blot analysis and real-time polymerase chain reaction assay (real-time PCR).Results Masson staining revealed significant myocardial fibrosis in rats exposed to radiation, while these changes were reduced when the rats were given Pio.Western blot analysis showed that the PPAR-γ protein expression in the heart tissue of irradiated rats were higher than in the non-irradiated group (F =12.435, P ＜ 0.05).Real-time PCR assay showed that PPAR-γ mRNA expression in the irradiation + Pio 20 mg· kg-1· d-1 group was higher than that in the Pio 20 mg· kg-1 ·d-1 group (F =2.333, P ＜ 0.05).The expression of TGF-β1 protein in the irradiation + placebo group were higher than those in the other five groups (F =17.578 ,P ＜0.05), and the CDK5 protein expression had a high level in the three irradiated groups while only the irradiation + placebo group was statistically higher than controls (F =3.651, P ＜ 0.05).Conclusions Pioglitazone may ameliorate radiation fibrosis in the rat heart through its anti-fibrotic activity, perhaps via inhibiting Cdk5-mediated PPAR-γ phosphorylation.

Objective:To investigate the effect on proliferation and apoptosis of T-cell leukemia cells by silencing NRP-1 ( Jurkat cells).Methods:The lentivirus plasmid which expresses NRP1 gene specific shRNA was constructed in our preliminary ex-perimental.We transfected the lentivirus plasmid to human T-cell Lymphoma cells.The proliferation of Jurkat cells different groups and effect on cell proliferation after chemotherapy drug EPI-treated were found by CCK-8 kit.The proliferation level and apoptosis rate of the cells were detected by flow cytometry and Annexin-V-FITC/PI method.Results:The proliferation level of NRP-1 /shRNA interference group was decreased significantly in 48 h,72 h,96 h,which was compared with the control groups.The apoptosis rate of the NRP-1/shRNA interference group was increased compared with control groups.The chemotherapy drug sensitivity of epirubicin ( EPI ) test results showed that EPI concentration was 0.025,0.05,0.1,0.2,0.4 μg/ml,the NRP-1/shRNA interference group of cell growth inhibition rate was increased,the corresponding control group difference had statistical significance(P<0.05).We choose the drug con-centration of the EPI IC50 for next experiments.NRP-1/shRNA interference group cell apoptosis rate increased significantly after induction,compared with the control groups difference was statistically significant ( P<0.05 ).Compared with control group, the expression level of Bcl-2 protein was decreased and the expression level of bax protein was increased significantly after EPI induction.The percentage of cells at G0/G1 phase increased significantly,while those at S phase decreased significantly.Conclusion:Plasmid shRNA-NRP1 inhibited the expression of NRP1 in Jurkat cells and decreased the proliferation level of Jurkat cells and promote their apoptosis and enhance their drug sensitivity;the molecular mechanism may relate to down-regulation of Bcl-2 and up-regulation of Bax.and arrested the cell cycle at G0/G1 phase.

BACKGROUND:There are many positive effects by activation of peroxisome proliferator activated receptor-gamma (PPARγ) signal pathway in cardiovascular system. Angiotensin II is closely related with myocardial fibrosis, however, there are few articles demonstrating that the activation of PPARγsignal pathway can weaken the expression of angiotensin II to improve the radiation-induced heart injury. OBJECTIVE:To evaluate the effect of angiotensin II type 1 receptor in the rat model of radiation-induced heart injury after PPARγsignal pathway is activated. METHODS:Sixty rats were randomly and equal y divided into five groups:control, pioglitazone, model, radiation+low-dose pioglitazone, radiation+high-dose pioglitazone. In the model, radiation+low-dose pioglitazone, radiation+high-dose pioglitazone groups, rats received 6 MV high energy X-ray irradiation at the range of 1.5 cm × 1.5 cm and the irradiation dose of 300 cGy/min, for 6 hours. Furthermore, rats in the radiation+low-dose pioglitazone and radiation+high-dose pioglitazone groups were given 10 and 20 mg/kg pioglitazone by lavage, for 30 days;rats in the model group were given 2 mL distil ed water. In the pioglitazone group, rats were treated with 10 mg/kg pioglitazone by lavage. RESULTS AND CONCLUSION:After rats were treated with pioglitazone, the heart injury and the heart fibrosis in the irradiated rats were decreased. The expressions of angiotensin II type 1 receptor mRNA and protein in the heart tissue were down-regulated. Experimental findings indicate that, pioglitazone intervention downregulates the expression of angiotensin II type 1 receptor in the rat models of radiation-induced heart injury and activation of PPARγsignal pathway al eviates the radiation-induced heart injury.