The study was aimed to investigate the effect of artesunate (ART) on the apoptosis of HL-60 cells in vitro and the expression of Bcl-2 and ICAD in the process of apoptosis induced by ART. The inhibition of ART on HL-60 cells were evaluated by means of MTT assay; cell apoptosis was detected by light microscopy, agarose gel electro-phoresis, flow cytometry; Western blot was used to analyze the expression of Bcl-2 and ICAD in cells during apoptosis induced by ART. The results showed that ART could significantly inhibit the proliferation of HL-60 cells in time-and dose-dependent manner. After treating HL-60 cells with ART for 48 hours, the IC(50) values was 18.33 microg/ml and its inhibition effect contributed to the induced apoptosis. Bcl-2 and ICAD proteins both all expressed in HL-60 cells, the level of expression declined as concentration increased. It is concluded that artesunate may induce apoptosis of HL-60 cells in vitro, Bcl-2 and ICAD may be an important control factor in the signal transduction pathway of ART-induced apoptosis.
Antineoplastic Agents, Phytogenic ; pharmacology ; Apoptosis ; drug effects ; Apoptosis Regulatory Proteins ; metabolism ; Artemisinins ; pharmacology ; HL-60 Cells ; Humans ; Proto-Oncogene Proteins c-bcl-2 ; metabolism

AlM:To investigate the effects of pirfenidone ( PFD) on the proliferation and transfomring growth factor-β1 ( TGF-β1 ) expression in vitro culture rat corneal stromal cells.METHODS: Corneal stromal cells from 8 to 10wk SD rats were isolated, cultured and treated with different concentrations of PFD 0mg/mL (control group), 0. 15mg/mL (experimental group▏), 0. 3mg/mL (experimental group‖), 1mg/mL (experimental group Ⅲ) for 48h. CCK-8 assay was performed to assess cell proliferation, while immunocytochemistry and Western Blot were used to detect the expression of ki-67 and TGF-β1 expression, respectively. RESULTS: Compared with control group, PFD significantly inhibited the proliferation in a dose -dependent manner ( all P < 0. 05 ), so was protein expression of ki-67. PFD significantly down-regulated the expression of TGF-β1 in a dose-dependent manner (P<0. 05).CONCLUSlON: Pirfenidone can significantly inhibit the proliferation of rat corneal stromal cell by down regulating TGF-β1 expression, therefore, it has potential prospect in lightening the corneal wound healing reaction.

Adolescent ; Adult ; Debridement ; methods ; Endoscopy ; Female ; Humans ; Male ; Middle Aged ; Neuroleptanalgesia ; methods ; Nose ; surgery ; Postoperative Period ; Young Adult

Adult ; Female ; Humans ; Nasal Cavity ; Nasal Lavage ; Nasal Obstruction ; prevention & control ; Pregnancy ; Pregnancy Complications ; prevention & control ; Rhinitis ; prevention & control ; Saline Solution, Hypertonic ; administration & dosage ; therapeutic use ; Young Adult

OBJECTIVEThe aim of this study was to observe the suppressive effect of bortezomib alone and the synergistic suppressive effect of bortezomib and adriamycin on the proliferation of the cell line Jurkat cells, and to discuss the mechanism of apoptosis induced by bortezomib.

METHODSThe suppressive effect of bortezomib and adriamycin on the proliferation of Jurkat cells in vitro was detected by MTT colorimetry, and the morphology of the cells was examined by histology. The cell apoptosis was measured by flow cytometry with Annexin V/PI staining and cell cycle analysis. The effect of bortezomib and adriamycin on the expression levels of caspase-3, caspase-8 and PARP were measured by Nestern blot.

RESULTSThe proliferation of Jurkat cells was significantly inhibited by bortezomib treatment (between 10 - 320 ng/ml) for 24 h, 48 h and 72 h, and the growing inhibition ratio showed a positive correlation with the drug concentration (r(24 h) = 0.900, P < 0.01; r(48 h) = 0.849, P < 0.01; r(72 h) = 0.679, P < 0.01), in a concentration-dependent manner. The IC(50) of Jurkat cells treated with bortezomib in a dose of 10 - 320 ng/ml was 137.64 +/- 6.82 ng/ml, but the IC(50) of Jurkat cells treated with bortezomib combined with adriamycin (125 ng/ml) for 24 h was significantly decreased to 20.44 +/- 2.85 ng/ml. The apoptosis rate had a positive correlation with the concentration of bortezomib (P < 0.01). After the Jurkat cells were treated with bortezomib, apparent shear bands of caspase-8, caspase-3 and PARP proteins were observed.

CONCLUSIONThere is an effect of Bortezomib to induce apoptosis in Jurkat cells, and the extrinsic pathway is one of the apoptosis-inducing mechanisms. There is a synergistic suppressive effect of the combination of bortezomib and adriamycin on the proliferation of Jurkat cells and enhances their chemosensitivity.

Antineoplastic Agents ; administration & dosage ; pharmacology ; Apoptosis ; drug effects ; Boronic Acids ; administration & dosage ; pharmacology ; Bortezomib ; Caspase 3 ; metabolism ; Caspase 8 ; metabolism ; Cell Proliferation ; drug effects ; Dose-Response Relationship, Drug ; Doxorubicin ; pharmacology ; Drug Synergism ; Humans ; Inhibitory Concentration 50 ; Jurkat Cells ; Poly(ADP-ribose) Polymerases ; metabolism ; Pyrazines ; administration & dosage ; pharmacology

Objective To master iodine nutritional status of people after universal salt iodization in Xining that reached the stage goal of elimination iodine deficiency disorders. Methods In the 7 counties investigated of Xining in 2009, 5 towns were randomly selected in each county, and one school was randomly selected in each town, 80 children aged 8 to 10 were randomly selected in each school, and goiter were examined, urinary iodine and salt iodine were tested. Thyroid gland goiter of children was detected by thyroid palpation, children's urinary iodine was tested by As( Ⅲ )-Ce4+ catalytic spectrophotometry, and salt iodine was tested by direct titration. Results A total of 2919 children aged 8 to 10 were examined, 31 goiter was detected, goiter rate was 1.06%(31/2919).One thousand and seventy-eight urine samples were detected, urinary iodine median was 205.3 μg/L, that lower than 20 μg/L accounted for 1.9% (20/1078), lower than 50 μg/L accounted for 4.5%(48/1078). Two thousand and seventy-nine salt samples were detected, median of salt iodine was 32.80 mg/kg, the rate of non-iodized salt was 0.87%(18/2079), the coverage rate of iodized salt was 99.13%(2061/2079), the qualified rate of iodized salt was 98.64% (2033/2061), the consumption rate of qualified iodized salt was 97.79% (2033/2079). Conclusions Prevention and control of iodine deficiency disorders has achieved remarkable results in Xining city, all indicators have reached the national standard to eliminate iodine deficiency disorders.

OBJECTIVETo detect novel mutations in the fibrillin 1 (FBN1) and transforming growth factor beta receptor type II (TGFBR2) genes by screening the genes from 14 patients with Marfan syndrome.

METHODSDenaturing high performance liquid chromatography (DHPLC) was introduced to screen for FBN1 and TGFBR2 mutations exon-by-exon. The DNA amplification fragments which DHPLC elution profiles showed different from the corresponding normal elution profile were sequenced to identify the positions and types of mutations. Restriction fragment length polymorphism (RFLP) was employed to further prove the mutations when needed.

RESULTSTwo gene mutations of the FBN1 were found in the patients with Marfan syndrome. They were a novel substitutional mutation (Intron29 +4A > T) of FBN1 and a recurrent nonsense mutation (8080C >T) of FBN1.

CONCLUSIONIntron29 +4A > T and 8080C > T of FBN1 are possibly the pathogenesis of the MFS patients.

Adolescent ; Base Sequence ; DNA Mutational Analysis ; Female ; Fibrillin-1 ; Fibrillins ; Humans ; Male ; Marfan Syndrome ; genetics ; Microfilament Proteins ; genetics ; Mutation ; Polymerase Chain Reaction ; Polymorphism, Restriction Fragment Length ; Protein-Serine-Threonine Kinases ; genetics ; Receptors, Transforming Growth Factor beta ; genetics

Adult ; Coronary Aneurysm ; complications ; Endocarditis, Bacterial ; complications ; Fistula ; complications ; Humans ; Male

Objective To investigate the myocardial damage in rats fed with corn from Keshan disease area added with bean puree. Methods Male Wistar rats were randomly divided into 3 groups according to their body weights, and fed with corn, corn from Keshan disease area added with bean puree, corn from non-endemic area. The GSH-Px activity of vena cardalis blood was examined in 1 and 3 months, rats were sacrificed after being fed for 6 months to examine the heart changes with HE stain. Results The three groups of GSH-Px activity were different in 1 and 3 months respectively(F=23.60,72.46, all P<0.01); GSH-Px activity was (181.58±22.15), (44.76±28.59)U/L in rats fed with corn, was (195.03±17.66), (30.38±3.35)U/L in those fed with corn added with bean puree from Keshan disease area, lower than the group fed with corn of non-endemic area[(340.90±95.42), (125.17±13.64)U/L, all P < 0.01]. But the difference of GSH-Px activity between simple corn group and corn adding bean puree groups of Keshan disease area was not obvious(P>0.05). Myocardial damage incidence of the three groups was 3/9,1/9,2/7. Difference among three groups did not have statistical significance(χ2=1.33, P> 0.05). Conclusions Only corn from Keshan disease area may induce myocardial damage pathology change. Adding bean puree into corn does not increase damage.

AIMTo explore the changes of MMP-2/9 protein expression and excitation in brain of repetitive hypoxic mice.

METHODSThe biochemistry techniques of SDS-PAGE, Western bolt and Gel Goc Image Analysis System were applied to determine the level of MMP-2 and MMP-9 expression and activation in cortex and hippocampus of mice. The animals were randomly divided into 5 groups: the normal control group (H0), acute hypoxic (H1, hypoxic exposure once), repetitive hypoxic groups (H2-H4, repetitive hypoxia for 2-4 runs respectively).

RESULTS(1) The MMP- 2 expression level was increased first then decreased in hippocampus and the significant decrease was found in H4 group (P < 0.05, n=6), but no significant changes among the 5 groups in cortex. In addition, no activated form of 66 kD MMP-2 had been detected both in hippocampus and cortex. (2) Along with the development of brain hypoxic preconditioning, the level MMP-9 protein expression also increased first then decreased gradually in hippocampus, and the significant changes were found both in H1 and H4 groups (P < 0.05, n=7 for each group). The same trace of changes was also found in the activation of MMP-9 (include 82 and 78 kD forms) in hippocampus, and the significance both in H1 and H4 (P < 0.05, n=7 for each group) were detected. However, there was not any significant change in the level of MMP-9 protein expression or activation to be found in cortex.

CONCLUSIONThese results suggested that MMP-2 and MMP-9 might play certain role in the development of cerebral hypoxic preconditioning, the different changes of MMP-2/9 protein expression and activation both in cortex and hippocampus might be involved in their selective vulnerability to hypoxia.

Animals ; Hypoxia, Brain ; metabolism ; Ischemic Preconditioning ; Matrix Metalloproteinase 2 ; metabolism ; Matrix Metalloproteinase 9 ; metabolism ; Mice ; Mice, Inbred BALB C