Animals ; Animals, Newborn ; Cell Hypoxia ; Cell Lineage ; Cell Proliferation ; Cells, Cultured ; Oligodendroglia ; cytology ; Rats ; Rats, Sprague-Dawley

Objective To explore the expressions of Survivin and VEGF and relationship between them in hepatocellular carcinoma(HCC).Methods The expressions of Survivin protein and VEGF protein in 50 HCC.30 cirrhosis and 10 normal tissues were assessed by immunohistochemical method.The expressions of Survivin mRNA and VEGF mRNA in 50 HCC,30 cirrhosis and 10 normal tissues were assessed by in situ hybridization.Results The expressions of Survivin and VEGF in cancer tissues,cirrhosis tissues,normal tissues weresignificantly different. The expression of Survivin in HCC tissues was stronger than that in cirrhosis,but the expreesion of VEGF in cirrho- sis was stronger than that in HCC tissues.Conclusion The expression of survivin.is closely associated with the ex- pression of VEGF in HCC and they take positive correlation.The abnormal expressions of Survivin and VEGF are closely associated with the development of HCC.They may play important roles in the development of HCC.

The expression of KAI1/CD82 and MRP-1/CD9 in transitional cell carcinoma of bladder (TCCB) and its clinical significance were investigated. Immunohistochemistry was used to detect KAI1/CD82 and MRP-1/CD9 protein expression in 52 TCCB specimens. Correlation between the expression of KAI1/CD82 and MRP-1/CD9 to clinicopathologic factors was statistically analyzed. The results showed that the positive rate of KAI1/CD82 and MRP-1/CD9 in TCCB was 50% and 61.5%, respectively. The MRP-1/CD9 and KAI1/CD82 expression was significantly associated with grade of TCCB (P<0.05), but no correlation was found between MRP-1/CD9 or KAI1/CD82 expression and clinical stage of TCCB (P>0.05). The expression level of MRP-1/CD9 and KAI1/CD82 in recurrent TCCB samples was lower than that in non-recurrent samples (P<0.05). Meanwhile, the correlation between the KAI1/CD82 expression and MRP-1/CD9 expression was statistically significant (r=0.316, P<0.05). It was concluded that KAI1/CD82 and MRP-1/CD9 expression may be important prognostic indicators and potentially useful for assessing the biological behavior of TCCB.

Bodily Secretions ; virology ; Humans ; Pharynx ; virology ; Pneumonia ; diagnosis ; virology ; Respiratory System ; virology

OBJECTIVETo investigate the effects of Shenqi Fuzheng injection (SQFZI) combined with docetaxcl, flurouracil and calcium folinate in treating advanced gastric carcinoma, and to evaluate the action of SQFZI for enhancing therapeutic effect and alleviating adverse reaction of chemotherapy.

METHODSSixty advanced gastric cancer patients were assigned to two groups randomly, the control group treated with chemotherapy alone and the treated group treated with SQFZI combined chemotherapy. Chemotherapy regimens (TFC) was given to all patients consisting of docetaxel 75 mg/m2 intravenous dripping on the 1st day, flurouracil (5-FU) 350 mg/m2 and calcium folinate (CF) 120 mg/m2 intravenous dripping with micro-pump continuously from day 1 to 5, for 21-28 days as a cycle. To patients in the treated group, starting from 3 days before chemotherapy, SQFZI 250 mL was dripped every day for 14 successive days. The clinic effects were evaluated after two-cycle treatment.

RESULTSThe short-term effective rate was 40.0% in the treated group and 33.3% in the control group. As compared with those in the control group, patients in the treated group after treatment had a higher Karnofsky score (chi2 = 7.21, P < 0.05) and body weight (chi2 = 11.47, P < 0.05), lesser adverse reactions in decreasing of peripheral blood leucocyte, damage of peripheral nerve, adverse reaction of gastrointestinal tract, as well as better immune function.

CONCLUSIONSQFZI could effectively improve the clinical symptoms induced by chemotherapy regimen TFC, alleviate the adverse reaction, raise patients' quality of life and their immune function.

Aged ; Antineoplastic Combined Chemotherapy Protocols ; administration & dosage ; therapeutic use ; Drug Therapy, Combination ; Drugs, Chinese Herbal ; administration & dosage ; therapeutic use ; Female ; Fluorouracil ; administration & dosage ; Humans ; Injections ; Leucovorin ; administration & dosage ; Male ; Middle Aged ; Phytotherapy ; Stomach Neoplasms ; drug therapy ; pathology ; Taxoids ; administration & dosage ; Treatment Outcome

Objective To investigate the in vitro effects of bladder cancer cell proliferation after silencing Notch1 gene. Methods The siRNA eukaryotic expression vector of Notch1 (psiRNA1)was constructed and transfected into bladder cancer cell lines T24 and BIU-87. Methabensthiazuron (MTT) and flow cytometry (FCM) assays were used to detect bladder cancer cells line growth, cell cycle and apoptosis after the transfection. RT-PCR and Western blotting were used to determine the expression changes of Notch1 in these cell lines. Results After transfection for 72 h, the rate of G0/G1 phase cells inceased from (23.89±1.32) % to (80.13±2.69)% in T24 cell line, and increased from (24.63±1.68)% to (69.44±2.41)% in BIU-87 cell line (both P<0.05). In addition, apop-totic cell index in T24 and BIU-87 cell lines increased from (1.28±0.14)% to (13.75±1.23)%, from (1.01±0.27)% to (8.72±1.01)%, respectively(both P<0.05). The growth of T24 and BIU-87 cell lines was obviously inhibited 24 h after the transfection, and the inhibitory effects lasted until 96 h after the transfection. Notch1 mRNA and protein significantly downregulated after transfection compared to the control(P<0.05). Conclusions Silencing Notch1 expression can inhibit the prolif-eration of bladder cancer cell lines. Notch1 gene might act as a tumor gene in bladder cancer.

AIMTo establish the model of oxygen-glucose deprivation in vitro rat hippocampal neurons.

METHODSThe hippocampal neurons cultured for 12 d were exposed to combined oxygen-glucose deprivation for 0.5-4 h and then cultured with original medium in normoxia for 24 h. Auto-biochemical analyzer determined LDH activity. The change of neuronal morphology and neuron survival were observed by converted contrast microscope and assessed by photography analysis system. Neuron apoptosis was detected by using the terminal deoxynucleotidyl transferase-mediated biotinylated deoxyuridine triphosphate nickel end labeling (TUNEL) method.

RESULTSThe neurons swelled, LDH release increased and neuron survival decreased after gradually oxygen-glucose deprivation. The percentage of apoptosis increased obviously 24 h after recovering the supply of oxygen and glucose.

CONCLUSIONThe model of oxygen-glucose deprivation in vitro rat hippocampal neurons is established successfully by using the modified ACSF (artificial cerebral spinal fluid) with serum and glucose free.

Animals ; Animals, Newborn ; Cell Hypoxia ; Cells, Cultured ; Glucose ; deficiency ; Hippocampus ; cytology ; Neurons ; cytology ; Oxygen ; physiology ; Rats ; Rats, Wistar

OBJECTIVETo study the effect of valproate acid sodium(VPA) on apoptosis of human gastric cancer cell BGC-823 and to explore its possible mechanism.

METHODSCell growth inhibition was examined by MTT assay. Apoptosis rate was detected by FCM with Annexin V/PI staining. The activities and protein expression levels of caspase 3, caspase 8 and caspase 9 were examined by spectrophotometry and indirect immunofluorescence technique respectively.

RESULTSThe growth inhibition rate and apoptosis rate of human gastric cancer cells, treated with 0.75-4.00 mmol/L VPA for 24 h and 48 h, elevated in time- and dose-dependent manner. Apoptosis rates of VPA 0.75 mmol/L 24 h and 48 h were (7.2 +/- 0.5)% and (9.2 +/- 1.0)%, of VPA 4.00 mmol/L 24 h and 48 h were (16.7 +/- 2.2)% and (20.4 +/- 1.6)% respectively, which were significantly different as compared to the control [24 h, (4.9 +/- 0.2)%, 48 h, (5.1 +/- 0.8)%] (P< 0.001). The activities and protein expression levels of caspase 3 and caspase 9 were up-regulated compared with the control group (P< 0.001), meanwhile the activity and protein expression of caspase 8 enhanced slightly after VPA treatment for 48 h.

CONCLUSIONVPA can inhibit the growth and induce the apoptosis of BGC-823 cells mainly through the activation of caspase 9 pathway.

Apoptosis ; drug effects ; Caspases ; metabolism ; Cell Line, Tumor ; Humans ; Stomach Neoplasms ; pathology ; Valproic Acid ; pharmacology

AIMTo study the protective effect of Quinacrine(QA) on rat striatum neurons from the injury caused by heat environment treatment, to probe the relationship between cell membrane injury and cellular injury protection, and to seek the possibility of QA as a preventive agent to heat injury.

METHODSPrimary cultured striatum neurons from newborn rats were pretreated with QA at different concentration for 1 h, and then heat-treated at 43 degrees C for another 1 h. Cell necrosis was detected by Trypan blue staining, and apoptosis was evaluated through Activated Caspase-3 dye and TdT dye.

RESULTSHeat treatment effected the survival of striatum neurons and resulted in great number of cell death, which was mainly mediated by cell necrosis process. It was shown that treatment of QA itself had little effect on the survival of striatum neurons, while QA pretreatment decreased cellular necrosis caused by following heat treatment.

CONCLUSIONQA protects striatum neurons from heat environment injury at about 20 pmol/L, and the protection may mediated by reduction of necrosis.

Animals ; Apoptosis ; drug effects ; Caspase 3 ; metabolism ; Cell Death ; drug effects ; Cells, Cultured ; Corpus Striatum ; cytology ; Heat-Shock Response ; Neurons ; drug effects ; Quinacrine ; pharmacology ; Rats ; Rats, Wistar