Objective: To study the plasma concentrations and pharmacokinetic parameters of 6,7 dimethoxycoumarin after oral administration of Herba Artemisiae Scopariae decoction and Yinchenhao decoction. Methods: A HPLC UV method was developed to determine 6,7 dimethoxycoumarin in rat plasma. The drug was extracted with acetonitrile from plasma and separated on a Kromasil ODS (250mm?4.6mm,5?m)column with methanol 1% solution of acetic acid THF (30∶63∶7) as mobile phase, UV detecter was set at 340nm. The data obtained were analyzed with Topfit program. Results: The liner calibration curves were obtained in the concentration range of 0.026～2.5 ?g?mL -1 . With non compartmental analysis, the main pharmacokinetic parameters after oral administration of Artemisiae Scopariae decoction and Yinchenhao decoction were as follows: T 1/2 was 1.30 and 1.75h, AUC 0→t was 1215.00 and 2527.85ng?h?mL -1 , AUC 0→∝ was 1325.90 and 2612.58ng?h?mL -1 respectively. Conclusion: This method can be used to study the pharmacokinetics of 6,7 dimethoxycoumarin derived from different traditional Chinese medicines containing this component.

This study was aimed to discuss the distribution and protein expression level ofμ-opioid receptor (MOR) in hippocampus of premenstrual syndrome (PMS) liver-qi stagnation rat model, in order to initially reveal the action mechanism of PMS liver-qi stagnation and intervention effect ofShu-Yu (SY) capsule. Chronic restraint stress method was used to copy PMS liver-qi stagnation rat model.SY capsule ofTiao-Gan prescription was given as intervention. Immunofluorescence (IF) and western blot (WB) technique were used to detect MOR in hippocampal CA1 and CA3 brain area of rats from each group. The results showed that compared with the normal group, the hippocampus MOR distribution arrangement was messy with increased protein concentration in the model group (P< 0.01). After drug intervention, the MOR protein level returned to normal level. It was concluded that the pathogenesis of PMS liver-qi stagnation may be associated with high expression of MOR in hippocampus CA1 and CA3 region of rats. SY capsule can effectively correct and restore it to nearly normal level. It may be one of the central mechanisms in SY capsule treatment of PMS liver-qi stagnation.

AIM: To investigate the anti-cancer effect of cytotoxic T lymphocytes (CTL) activated by sensitized dendritic cells (DCs). METHODS: Immature DCs were induced in vitro from peripheral blood monocytic cells (PBMC) and sensitized by adding tumor cells antigen extract. DCs were identified by their morphology and surface markers. MTT assay was used to evaluate the killing activity of CTL activated by sensitized DCs. The effects of specific CTL cells on inhibiting transplanted tumor HT-29 growth and on preventing HT-29 tumor generation were evaluated by injecting CTL into nude mice. RESULTS: After cultured for seven days, a large number of activated DCs were obtained with typical morphology, extensive stimulatory proliferation capacity and high CD80 (63.5%), CD83 (67.6%) and CD3/HLA-DR (83.2%) expressions. The killing activity of CTL at 20∶1 ratio of effective cells to target cells was more than 75% to tumor cells, 35%-45% to homologous cell line and weaker to other germ cell line (P

Animals ; Central Nervous System Diseases ; drug therapy ; Drug Design ; Drugs, Chinese Herbal ; Humans ; Inflammation ; drug therapy

Japanese encephalitis virus (JEV) is a single-stranded and positive-sense RNA, which has a single ORF (open reading frame), encoding a polyprotein precursor. Non-structural protein 3 (NS3) plays an important role in processing the polyprotein precursor and has become an important drug target of flavivirus. In this study, NS2BH-NS3 gene was amplified by PCR and subcloned to the prokaryotic expression plasmid, resulting pET30a-NS2BH-NS3. The fusion protein was expressed in Escherichia coli BL21 (DE3) in soluble form after induction by Isopropyl beta-D-1-Thiogalactopyranoside (IPTG). The recombinant protein was purified by Ni-NTA affinity column. Then a fluorescence resonance energy transfer (FRET) method was used to determine enzymatic activity and the assay conditions were optimized. After screening 113 compounds, we found two compounds inhibiting the activity of NS2BH-NS3. This study provides a convenient and cost-effective method for screening of JEV NS3 protease inhibitor.
Encephalitis Virus, Japanese ; enzymology ; Escherichia coli ; metabolism ; High-Throughput Screening Assays ; Protease Inhibitors ; chemistry ; RNA Helicases ; metabolism ; Recombinant Fusion Proteins ; metabolism ; Serine Endopeptidases ; metabolism ; Viral Nonstructural Proteins ; metabolism

Animals ; Embryo Culture Techniques ; Embryo, Mammalian ; Female ; Ganglia, Spinal ; cytology ; drug effects ; Glial Cell Line-Derived Neurotrophic Factor ; pharmacology ; Male ; Motor Neurons ; drug effects ; Neurons, Afferent ; drug effects ; Rats ; Rats, Sprague-Dawley

BACKGROUND:Kinesin II family member 3A (KIF3A), as an important member of the kinesin-2 family, not only holds some general characters of kinesin including the regulation of intracel ular transport and mediation of microtubule movement, but also possesses its own specific features.
OBJECTIVE:To review the research progress of the function of KIF3A recently.
METHODS:A computer-based online research for relative literatures published from January 1996 to July 2016 was performed in PubMed and CJFD databases using the English retrieval words of“KIF3A;kinesin;molecular motor”and Chinese keywords of“kinesin;microtubule;function;molecular motor;spinal cord injury”, respectively. A total of 92 articles were retrieved, and 62 eligible articles were included according to the inclusion criteria.
RESULTS AND CONCLUSION:KIF3A is involved in new bone formation regulation, in the control of nephron number, cell survival and gene expression, in sperm formation and in the inhibition of prostate cancer and glioblastoma process:In the meanwhile, whether KIF3A is involved in spinal nerve injuries is discussed. All provide valuable new information and new ideas for further in-depth study on the KIF3A.

Objective To assess the relationship between serum uric acid (SUA)and metabolic syndrome and coronary artery disease(CAD).Methods 232 untreated subjects with essential hypertension were divided into two groups(CAD and no CAD)by coronary angiography.All subjects were free of myocardial infarction,cardiomyopathy,valvular disease, atrial fibrillation,aortic dissection,and renal disease.Results Compared to no CAD group,age,diabetes,triglycerides and SUA in CAD group were higher.There was a significant association between SUA and the severity of CAD (P=0. 015).However,after adjustment for concomitant risk factors of cardiovascular disease,SUA was not an independent risk factor of CAD(P=0.151).In sex-specific analysis,there was a trend of SUA to be an independent risk factor of CAD in women(P=0.062),but it was no statistic significance.The highest quartile level of $UA tended to be associated with increased risk for CAD,but it was not statistically significant either(OR=2.52,P=0.075).SUA was closely associated with metabolic syndrome and diabetes in woman.Conclusion In untreated patients with essential hyperteusion,SUA was associated with metabolic syndrome and the severity of CAD,but it is not an independent risk factor of CAD,the raised SUA may be only a marker of insulin resistance.

Objective To explore the inhibiting effects of arsenic trioxide and cisplatin on MG-63 cells. Methods Using MTT assay,flowcytometry,phase contrast microscopy and electron microscopy methods,the therapeutic effect of arsenic trioxide was studied for the osteosarcoma in the cultured MG-63 cells in vitro,and compared these effects with cisplatin. The inhibitory rotes of cell growth and the effect of apoptosis and cell cycle were compared between arsenic trioxide and cisplatin on MG-63 cells. Results The contrast phase microscope revealed the adhesion ability of normal groups was good and cellular morphology showed epithelium cells. But the celhdar morphology showed irregular arrangement in arsenic trioxide groups and cytoplasmic vacuoles in cisplatin group. Electron microscope revealed the globular plasmalemma ecphymas in cell surface of control groups,the enlarged crista mitochondriales and the double-deck membrane structure appeared clearly. But electron microscope revealed globular plasmalemma processes in cell surface of arsenic trioxide groups,thinned crista mitochondriales and clearly seen karyopycnosis and nuclear membrane of apoptotic cells. The globular plasmalemma processes in cell surface of cisplatin groups were separated,nuclear membrane thickened and chromatin were in sandy shape. Both arsenic trioxide and cisplatin inhibited effectively MG-63 cells growth. There was a significant difference in different groups of inhibition ratios to the growth of cells(all P < 0.05). In 2,4,8,16,32,64,128 hours,the inhibition ratios(%) of arsenic trioxide(56.31±0.03,70.00±0.06,79.84±0.03,87.31±0.13,84.70±0.09,90.68±0.06,91.18±0.05) and cisplatin groups(7.55±0.15,15.70±0.17,30.72±0.07,49.80±0.05,45.11± 0.13,61.62±0.08,93.80±0.12) were obviously increased as compared with those in the control group(2.03± 0.07,2.78±0.08,3.11±0.01,5.67±0.04,12.23±0.04,18.65±0.04,24.45±0.04,all P < 0.05). Moreover the inhibition ratio of arsenic trioxide group in 2 to 32 hour was significantly higher than that of cisplatin group and the effect was more faster(all P < 0.05). Both arsenic trioxide and cisplatin could induce apoptosis MG-63 cells. There was a significant difference in different groups of the inhibition ratio to the growth of cells(F = 13.317,P < 0.05). The inhibition ratios(%) of arsenic trioxide on 24,36,48 hour(20.50±3.78,45.76±9.90,25.16±15.41),and cisplatin groups on 24,36,48 hour(12.55±1.51,18.85±3.40,12.37±5.43),were obviously increased as compared with those in the control group at the same time(6.57±1.48,8.03±2.08,6.54±1.30,P< 0.05 or<0.01). Both arsenic trioxide and cisplatin inhibited MG-63 cells cycle. There was a significant difference in different groups of the inhibition ratio to the growth of cells(F = 54.579,43.429,21.795,P < 0.05 or < 0.01). And the total inhibition ratios(%) in G1 cycle of arsenic trioxide(78.26±5.24) and cisplatin groups(80.48±2.81) were obviously increased as compared with those in the control group(57.49±6.65,all P < 0.05 or < 0.01). Conclusions Arsenic trioxide and cisplatin can effectively inhibit the proliferation of MG-63 cell line and induce the apoptosis of MG-63 cell line. And the effects induced by arsenic trioxide group were faster than that of cisplatin groups. Moreover arsenic trioxide can arrest the cell cycle of MG-63 cell line at G1 phase.

Objective To analyze the reasons of perioperative hypoxia in Stanford A aortic dissection,and summarize its management strategies.Methods From Dec.2005 to Jul.2011,sixty four patients underwent surgery for acute type A aortic dissection,of which 9 cases were with chronic dissection and 55 cases with emergent ones.Preoperative oxygen fraction ratio( PaO2/FiO2 )in 51 cases was lower than 200 mm Hg.All of them underwent the surgery with the help of deep hypothermia cardiac arrest technique.Results Three cases died.Thirty-three cases could not live without ventilation during the first 72 h because of continuous hypoxia ( PaO2/FiO2 ＜ 200 mm Hg).One case underwent tracheotomy and auxiliary ventilation for 9 days.The rest were live without ventilation after auxiliary ventilator for 72 - 120 hrs.The data showed that postoperative hypoxia was related to preoperative hypoxia (oxygen fraction ratio ＜ 200 mm Hg),BMI,acute onset,hypothermia cardiac arrest time,and transfusion more than 3000 ml ( P ＜ 0.05 ).Conclusion Great attention should be paid to the perioperative hypoxia-related factors in Stanford A dissection,which will be helpful to improve prognosis.