Objective: To study the inhibitory effects of periplocin from cortex periplocae (CPP) on proliferation of human esophageal carcinoma TE-13 cells and the related mechanism for cell cycle arrest. Methods: The inhibitory effects of CPP on the growth of TE-13 cells were measured by MTT assay. The morphological changes of TE-13 cells were analyzed by Gimsa staining. Detection of cell apoptosis and cell cycles were performed by flow cytometry. Protein expressions of cyclin-dependent kinase CDK2 and CDK4 were analyzed by Western blotting assay. Results:CPP significantly inhibited the proliferation of TE-13 cells in a dose- and time-dependent manner (P < 0.01). After treatment with CPP for 48 h, the IC50 was 0.61 μg/mL. TE-13 cells showed morphologic changes of apoptosis after treatment with CPP 2 μg/mL for 48 h. The proportion of cells in G0/G1 phase significantly increased (P < 0.01) and the number of cells in S phase decreased (P < 0.01). The proportion of cells in G2/M phase had no significant difference before and after CPP treatment (P > 0.05). CDK4 expression was inhibites by CPP at different concentrations, but the expression of CDK2 had no marked changes (P > 0.05). Conclusion: CPP significantly inhibites the growth of TE-13 cells. The action mechanism may be related with induction of cell cycle blocking and apoptosis.

Embolism, Paradoxical ; complications ; Female ; Humans ; Middle Aged ; Myocardial Infarction ; etiology

Objective To investigate the optimal mild hypothermia course and cerebral temperature of the neonatal rats after hypoxic-ischemic brain injury. Methods The posthypoxic-ischemic rats of experimental group (n=60) were placed in the glass jars immeresd in water bath held constaut at either 29 C or 3l C for 24h, 48h or 72h. While the rats of room temperature group (n=22) were stayed in room air. Blood glucose, blood gases and neuropathology findings were studied to determine the therapeutic effects. Results The brain temperature droped 3C or 5C when enviro ment temperature was 31C or 29C respectively. The blood glucose remained normal. Neuropathology findings reveled that the brain damage of experimental rats reduced 46%～86% compared to the room temperature group. Conclusion Reducing the cerebral temperature by 4～5 C for 72 hours after hypoxic-ischemic brain injury can lead to superior protective effect.

Objective To study the effects of Lipoxins A4(LXA4)on the expressions of aquaporin(AQP)1,3,5 in type Ⅱ pneumonocytes(ATⅡ)of rat treated with lipopolysaccharide(LPS).Method One pathogenfree male Spree Dawley(SD)rat every time.weighing 200～250 g,were used for the study.The typeⅡpenumonocytes of rats were isolated and purified,and the changes of cellular ultrastructure were observed by electron microscope in order to get the purity quotien＞90%.The type Ⅱ pneumonocytes were divided randomly into five groups,namely,vebicukun group(alcohol 0.7μL/mL),control group,LXA4 group(1×10-7mol/mL),endotoxin group(LPS 1μg/mL)and LXA4+LPS group(LXA4 1×10-7mol/mL,LPS 1μg/mL).AQP-1,3,5 mRNA of in the typeⅡpenumonocytes were assayed by using reversal transcription poly chain reaction(RT-PCR),and the expressions of AQP-1,3,5 protein were detected by using.immunohistochemistry(IHC).One each specimen,these tests were repeated for six times.ANOVA was used for statistical analysis.Results RT-PCR and IHC showed that when AT Ⅱ treated with 1 μg/mL LPS for 4 hours,the AQP-1,3,5 mRNA and the expressions of AQP-1,3,5 protein were significantly decreased in LPS group compared with control group(P＜0.01).However,the AQP-1,3,5 mRNA and the expressions of AQP-1,3,5 protein after application of LXA4 significandy increased in LPS+LXA4 group in comparison with LPS group(LPS+LXA4,AQP1:0.647±0.132,AQP3:0.900±0.856,AQP5:0.879±0.058;LPS,AQP1:0.297±0.133,AQP3:0.512±0.113,AQP5:0.647±0.110;P＜0.01).The AQP-1,3,5 mRNA and the expressions of AQP-1,3,5 protein were aignificandy increased in LXA4 group in comparison with control group(LXA4,AQP1:0.539±0.142,AQP3:0.818 4-0.176,AQP5:0.841±0.066;Blank Control,AQP1:0.518±0.139;AQP3:0.138±0.136,AQP5:0.766±0.066;P＜0.01).Conclusions AQP-1,3,5 exist in typeⅡpenumonoeyte of rata,and the LXA4 can up-regulate the mRNA and protein expressions of AQP-1,3,5 in Type Ⅱ penumonocytes of rats treated with LPS.

Adolescent ; Child ; Child, Preschool ; Colitis, Ulcerative ; pathology ; Colonoscopy ; Female ; Humans ; Infant ; Male

Abortion, Habitual ; drug therapy ; immunology ; Antibodies, Anticardiolipin ; blood ; Aspirin ; administration & dosage ; Drug Therapy, Combination ; Drugs, Chinese Herbal ; therapeutic use ; Female ; Heparin ; administration & dosage ; Humans ; Integrative Medicine ; methods ; Prednisone ; therapeutic use ; Pregnancy

MicroRNAs (miRNA) plays an important role in biological development and disease occurrence and development, and acts as a "main switch" in biology. Among patients of essential hypertension, around 1/3 would suffer left ventricular hypertrophy (LVH). Hence, essential hypertension becomes an independent risk factor for cardiovascular diseases. And miRNAs plays an important role in the occurrence and development of LVH. This paper reviewed the role of miRNA in regulating the stress signaling pathway, defined its impact on the occurrence of LVH, and further emphasized the opportunities and challenges of miRNA as a biomarker and therapeutic target.
Essential Hypertension ; Humans ; Hypertension ; complications ; genetics ; Hypertrophy, Left Ventricular ; complications ; genetics ; MicroRNAs ; genetics ; Risk Factors ; Signal Transduction ; genetics

ObjectiveTo observe the changes of amplitude-integrated electroencephalogram (aEEG)of neonatal asphyxia with different Apgar scores,and to investigate the diagnostic value of aEEG for hypoxicischemic encephalopathy(HIE) in neonatal asphyxia.MethodsaEEG monitoring were detected on 56 fullterm asphyxia neonates who were hospitalized in our neonatal department from Dec 2010 to Oct 2011.According to 1 minute Apgar score after birth,56 cases were divided into two groups:observation group in which 36 cases with Apgar score 0～7,and control group in which 20 cases with Apgar score 8～10.aEEG monitoring was done within 6 h,2 d,3 d,7 d of each neonates after birth,and the changes of aEEG were analyzed and the diagnostic value on HIE were evaluated.ResultsAmong 20 cases in the control group,the aEEG results in 6 hours after birth were 17 cases (85％) had normal aEEG results,3 cases( 15％ ) mildly abnormal,nd no one severely abnormal.The aEEG results of patients in observation group(36 cases) were 18 cases(50％ ) had normal aEEG results,13 cases(36.1％ ) mildly abnormal,and 5 cases( 13.9％ ) severely abnormal.The abnormal rate in observation group was significantly higher than that of the control group ( x2=5.3,P＜0.001 ).There were 34 HIE patients in the total 36 cases of observation group,whose aEEG monitoring results in 6 hours after birth were associated with HIE clinical grading( Spearman's rank correlation coefficient was 0.867,P＜0.01 ).Dynamic aEEG monitoring for 56 patients showed that 21 cases had abnormal aEEG in 6 hours after birth,in whom 15 cases(71.4％ ) could returned to normal after 48～72 hours after birth,and there were only 4 case (7.1％ ) still had severely abnormal aEEG results in the seventh day after birth.ConclusionThe aEEG dynamic monitoring for full-term HIE neonates after birth enhances early prediction of HIE.

Objective By making models of premature animal,explores the effects of dexamethasone on the brain development of premature rats and its mechanisms.Methods Eighteen SD rats were randomly divided into high-dexamethasone(H-Dex) group,low-dexamethasone (L-Dex) group and normal saline(NS) control group,with 6 rats in each group.The pregnant rats in L-Dex group were injected with dexamethasone [0.1 mg/(kg·d)] from 16 to 18 days of pregnancy,while the pregnant rats in H-Dex group were injected with dexamethasone [0.5 mg/(kg· d)] ; the pregnant rats in NS control group were injected with 0.9％ NaCl of the same volume.All of the fetal rats were received after administrating caesarean operation on the day 19 of pregnancy.Rats were sacrificed at the directed time and brain tissue was prepared.Histological feature and the water content of the brains were observed.Level of apoptosis was measured by flow cytometry.The expressions of myelin basic protein (MBP) and interleukin(IL)-1β in brain tissue homogenate were detected by ELISA.Results (1) The brain water contents of rats in H-Dex group,L-Dex group and NS control group were (85.94 ± 0.54) ％,(86.08 ± 1.01) ％,(86.94 ± 0.82) ％.Compared with NS control group,the water contents of Dex group were lower (P ＜ 0.05).(2) Glial cells of brain cortex in L-Dex group and H-Dex group were more mature than in NS control group,and the changes in H-Dex group was more significant.(3) The expressions of MBP in brain tissue of H-Dex group,L-Dex group and NS control group were (5.73 ± 1.06) μg/mg,(5.46 ±0.77) μg/mg and (2.42 ±0.52) μg/mg.Compared with NS control group,Dex group was higher(P ＜0.05).While the expressions of IL-1β in brain tissue of H-Dex group,L-Dex group and NS control group were (249.05 ± 11.29) pg/g,(257.47 ± 9.33) and (292.66 ± 21.51) pg/g.Compared with NS control group,Dex group was lower(P ＜ 0.05).There was no significant difference between H-Dex group and L-Dex group(P ＞ 0.05).(4) The level of apoptosis in H-Dex group,L-Dex group and NS control group were (18.07 ± 1.63) ％,(6.88 ± 0.47) ％ and (2.00 ± 0.32) ％.Compared with NS control group,the level of apoptosis in Dex group was higher(P ＜0.05),and H-Dex group was higher than that in L-Dex group.Conclusion (1) Using dexamethasone prophylactic could promote the development of glial cells,reduce the water content,increase the expressions of MBP,and decrease the expressions of IL-1β in brain tissues.It indicates that dexamethasone may play a major role in maturation of fetal brain.(2) Using dexamethasone prophylactic could increase the amounts of the apoptosis cells,and this effect is dose-dependent.It indicates that dexamethasone may have a negative effect on the fetal brain and suggestes that using dexamethasone in premature infant should be cautious,and if it has to,using a lower dose.

Objective To investigate the effect and mechanism of phosphorylated protein kinase R-like ER kinase(p-PERK) and C/EBP homologous protein(CHOP) after hypoxic-ischemic brain damage ( HIBD) . Methods Neonatal 7-day-old Sprague Dawley rats were divided into sham-operation control group and HIBD group( n=30 per group) . Each group was divided into 0 h,6 h and 24 h subgroup after operation ( n=10 per group) . The ratio of apoptosis of brain cell was measured by flow cytometer and the expression of p-PERK and CHOP were detected by Western blot. Results (1)Apoptosis cell appeared at 6 h in HIBD group,the ratio of cell apoptosis was(2. 17 ± 0. 19)%. The apoptosis cell obvious increased at 24 h,the ratio of cell apoptosis was(13. 42 ± 0. 83)%. There was a significant increase in the ratio of apoptosis after HIBD 6 h and 24 h, as compared with sham-operation control group [ ( 0. 57 ± 0. 06 )%( P <0. 01 ) ] . ( 2 ) The expression of both p-PERK and CHOP was very low in sham-operation control group. In the HIBD group,the expression of both p-PERK and CHOP began to increase at 6 h and increased furthermore at HIBD 24 h. The differences in the expression levels of p-PERK and CHOP in HIBD group among different time points were significant( P<0. 01 ) . ( 3 ) The expression of p-PERK positively correlated with the expression of CHOP (r=0. 997,P< 0. 05). Conclusion With the emerging of apoptosis after HIBD,the expression of both p-PERK and CHOP increases. The imbalance in the expression of PERK induces the apoptosis of brain cells in the HIBD of neonatal rats by regulation of CHOP expression.