The early characterization of the diazepam-binding sites outside the brain led to their assignment as peripheralbenzodiazepine receptors, or PBRs, to distinguish them from the central benzodiazepine receptor.Although PBR is a widely used and accepted name in the scientific community,recent data regarding the structure and molecular function of this protein increasingly support renaming it to represent more accurately its subcellular role (or roles) and putative tissue-specific function (or functions). Translocator protein (18 ku,TSPO), is proposed as a new name, regardless of the subcellular localization of the protein. This review deals with the pharmacological, structural and molecular characterization of the PBR and its role in the neuropshcopharmacology.

Objective To analyze labor duration in nulliparous women and discuss the change about curve of labor duration. Methods Two thousand, one hundred and forty nulliparous, full-term pregnant, singleton, cephalic presentation and vaginal delivery women who delivered at Peking University First Hospital were included. There were 1 300 cases between January 1, and December 31, 2009, while 840 cases between January 1, and May 31, 2013. A retrospective study was conducted. Data on maternal age, gestational age at delivery, body mass index at delivery, newborn weight, time of labor initiation, cervical dilatation and the amount of bleeding within the first 24 h after delivery were recorded. Data were compared by t test and χ2 test. The median time span corresponding to one-centimeter-increase in cervical dilatation was calculated. Results (1)Compared with data from 2009, the maternal age [(29.0±3.0) vs (29.6±2.8) years, t=4.77], incidence of postpartum hemorrhage [1.8%(24/1 300) vs 4.3%(36/840),χ2=11.17], proportion of induced labor [37.3%(485/1 300) vs 64.0%(538/840),χ2=146.23] and proportion of analgesia during labor [54.2%(705/1 300) vs 61.5% (517/840), χ2=11.15] were all higher in 2013 (all P<0.01). (2)The median (minimum–maximum) time span corresponding to a one-centimeter-increase in cervical dilatation was 3-4 cm which corresponded to 2.2 h(0.8-4.3 h), 4-5 cm which corresponded to 1.9 h(0.6-4.0 h), 5-6 cm which corresponded to 1.8 h(0.5-4.0 h), 6-7 cm which corresponded to 1.6 h(0.5-2.0 h), 7-8 cm which corresponded to 1.8 h(0.8-2.0 h), 8-9 cm which corresponded to 1.3 h(0.2-2.5 h), and 9-10 cm which corresponded to 0.6 h(0.1-2.5 h). The curve of labor duration showed a slow uptrend with time on the horizontal axis and cervical dilatation on the vertical axis. Conclusions The curve of labor duration exhibits a slow uptrend with neither an acceleration phase nor a deceleration phase. It is important to redefine the time span of labor duration in China for appropriate clinical treatment.

Objective To observe the effects of intensive training at different intensities on the expressions of semaphorin 3A ( Sema 3A) and its receptor neuropilin ( NP-1 ) and the cell apoptosis in cerebrum after cerebral ischemia-reperfusion in rats,and to investigate the possible mechanism of intensive training in recovery of motor function after cerebral ischemia-reperfusion in rats.Methods To establish animal model of cerebral ischemia-reperfusion in rats,the intraluminal thread method was applied to cause left middle cerebral artery occlusion (MCAO) for 2 h and before reperfusion.After cerebral ischemia-reperfusion model were established for 24 h,60 male model Wistar rats were randomly divided into training group 1 ( swimming for 5 min once a day),training group 2 ( swimming for 10 min once a day),training group 3 (swimming for 10 min twice a day) and control group (no training) ; another 15 rats assigned to the sham-operation group were subject to no MCAO and no training.Neurological function was evaluated by Garcia scores,and terminal deoxynucleotidyl transferase mediated deoxyuridine triphosphate-biotin nick end labeling (TUNEL) was performed to dectect the cortical cell apoptosis.Expressions of neural growth inhibition factor Sema 3A and its receptor NP-1 were detected by immunohistochemistry.Results The neurological function in sham-operation group was normal.The differences of Garcia scores at different time points beween sham-operation group and control group were significant (P ＜ 0.01 ).Garcia scores in all training groups,were significantly higher than those in controls at the 7th and 14th d after swimming training ( P ＜ 0.01 ),especially in training group 3 the Garcia scores were ( 12.80 ± 0.45 ),( 15.20 ± 0.45 ),( 16.80 ± 0.45 ),respectively,at the 3rd,7th and 14th d after swimming training.The rates of positive cell of Sema 3A,NP-1 and TUNEL indexes in all training groups were lower than those in controls at the 3rd,7th and 14th d after swimming training (P ＜ 0.01 ),especially in the training group 3.At the 3rd,7th and 14th d after swimming training in training group 3,the rates of TUNEL indexes positive apoptosis cells were ( 29.43 ± 1.38 ) ％,( 22.30 ± 1.21 ) ％,( 17.58 ± 1.70) ％,respectively,the positive cell rates of Sema 3A were ( 19.64 ± 1.17) ％,(9.73 ± 3.83)％,(8.24 ± 0.87)％,respectively,the positive cell rates of NP-1 were ( 33.95 ± 6.86) ％,( 27.95 ± 1.29 ) ％,( 18.90 ± 1.44 ) ％,respectively,the reduction of positive cells expressions in training group 3 was significantly more obvious compared with other training groups (P ＜ 0.01 or 0.05).Conclusions Rehabilitation training can reduce the expression of positive cell of Sema 3A,NP-1 and TUNEL indexes in rats after cerebral ischemia-reperfusion and can improve motor function recovery and facilitate neural plasticity.The more intensive the training,the better the effects.

ObjectiveTo investigate the protective effects of epigallocatechin gallate (EGCG) in a mouse model of Parkinson's disease induced by 1-Methyl-4-phenyl-1,2,3,6 tetrahydropyridine (MPTP).Methods32 C57BL/ 6 male mice were randomly divided into 4 groups: Model group was administrated with 16 mg/kg MPTP (i.p., four times, 2 h interval); Sham group was treated with saline; EGCG treatment group was given EGCG (5 mg/kg) after MPTP administration; normal group was just given EGCG (5 mg/kg) as treatment group. After given EGCG for 3 weeks, behavioral tests, tyrosine hydroxylase (TH) immunohistochemistry staining and the HPLC for dopamine (DA) and its metabolites were used.ResultsThe present results indicated that oral administration of EGCG significantly improved the behavioral impairement in mice induced by MPTP (P<0.05). And in the EGCG treatment group, there were more TH-positive neurons than in model group. In addition, levels of DA and its metabolites in striatum decreased significantly in MPTP group (P<0.05). Though the concentration of DA and its metabolites in EGCG treatment group tended to increase, however, there was no significance between EGCG treatment and model group.ConclusionEGCG could improve the behavioral impairment in a mouse model of Parkinson's disease induced by MPTP and protect against the loss of the dopamine neurons in the substantia nigra (SN).

ObjectiveTo evaluate the quantitative and qualitative changes of peripheral-type benzodiazepine recepors (PBRs) in brain mitochodria and in platelet membrane in aging rats. MethodsMale Sprague-Dawley rats were divided into 3- and 24-month groups. All animals were sacrificed by decapitation and the brains were immediately removed. Mitochondrial components from dissected cerebral cortex were isolated. The membrane of platelets from venous blood was prepared by the method of hypotonic hemolysis. The specific binding assay of the radioactive PBRs antagonist ［3H］PK11195 to membrane was performed. Scatchard analysis was performed to estimate the equilibrium dissociation constant (Kd) and the maximal binding site density (Bmax). ResultsA significant increase in ［3H］PK11195 binding activity in the mitochodria from cerebral cortex in 24-month rats was observed compared to that in 3-month rats(P<0-001). Meanwhile, the Scatchard analysis revealed that there was an increase in Bmax, with a significant increase in Kd in 24-month rats. The same change of ［3H］PK11195 binding activity was noted for platelet membrane in 24-month rats(P<0-001).ConclusionThe density of PBRs increases in cortex mitochondria in aging rats, but the binding affinity of PBRs decreases which may be attributable to the progressive pathogenesis of aging in rats. ［3H］ PK11195 binding activity of platelet membrane might reflect the change of PBRs in the brain tissue.

ObjectiveTo observe the effects of Jiuqiang Naoliqing(JNQ) on the microcirculation of the cheek pouch of golden hamsters. MethodsAutomatic measuring device was used to evaluate the changes of microcirculation. ResultsAfter the disorder of microcirculation of cheek pouch made by noradrenaline(NA), the JNQ group recovered better and more rapidly than other groups. ConclusionJNQ can prevent and reverse the disorder of microcirculation made by NA, and do better than NQ.

OBJECTIVE To study the molecular mechanism of cisplatin(DDP)by which HeLa cell growth and proliferation are inhibited. METHODS Cultured HeLa cells were treated with DDP 0.02-75 μmol · L-1 for 24 or 48 h. CCK-8 assay was used to determine the cell proliferation. The wound scratch assay was used to detect the cell migration and invasion. Flow cytometry was used to detect the cell cycle arresting. q-PCR was used to test the expression of metastasis suppressor gene 1 (MTSS1)mRNA. Western blot was used to determine protein levels of MTSS1,phosphorylated-extra?cellular signal-regulated kinase(p-ERK) and phosphorylated-serine-threonine kinase(p-AKT). RESULTS Following the treatment with DDP for 24 or 48 h,the proliferation of HeLa cells was inhibited significantly (P<0.05),the value of the half inhibitory concentration (IC50) of cells was 4.14 and 11.82 μmol · L-1. Migration and invasion activity of HeLa cells were reduced according to the wound scratch assay(P<0.05). Flow cytometry results showed that the cell cycle was arrested at S phase. q-PCR results showed that MTSS1 mRNA expression changed with DDP in a concentration-dependent manner (r24 h=-0.965,P<0.01;r48 h=-0.953,P<0.01). Western blot showed that the protein levels of MTSS1,p-ERK and p-AKT expression declined significantly with the increase in DDP concentrations(p-ERK:r24 h=-0.875,P<0.01;r48 h=-0.966,P<0.01. p-AKT:r24 h=-0.831,P<0.01;r48 h=-0.863,P<0.01. MTSS1:r24 h=-0.969,P<0.01;r48 h=-0.988,P<0.01). CONCLUSION DDP treatment inhibits HeLa growth and proliferation by interfering with the MTSS1 expression and disturbing the activation of ERK and AKT signaling pathways.

Objective To investigate the effect and its mechanism of diazoxide on the blood-brain barrier (BBB) of rats after cerebral ischemia/reperfusion (I/R) injury.Methods Sixty Wistar rats were randomly divided into sham operation group,I/R group,and diazoxide pretreatment groups of low,middle,large dose (5,10,20 mg/kg).The I/R models of rats were performed to undergo middle cerebral artery embolism by thread.BBB permeability was estimated by Evans blue (EB) dyeing,transmission electron microscope (TEM) was used to observe the modification of interendothelial tight junction (TJ) of capillaries.The expression of aquaporin-4 (AQP4) in every rat brain tissues was detected by immunity histochemistry technique.Results (1) Compared to sham operation group,the permeability extent of EB were significantly increased by I/R,which was distinctly attenuated in middle and large dose of diazoxide pretreatment rats,while no obvious changes were found between I/R and low dose groups.(2) TEM showed that TJ of the brain tissue opened after I/R injury and no significant opening of TJ was observed in middle and large dose of diazoxide preconditioning groups.(3) Compared to sham operation group,the expression of AQP4 in the brain tissue of the I/R group was apparently increased (P ＜0.01).Compared to I/R group,the expression of AQP4 was apparently increased in middle and large dose pretreatment groups (P ＜ 0.01),and there were no obvious difference between low dose group and the I/R group.Conclusions Preconditioning of ischemia/reperfusion injury with diazoxide protects the blood-brain barrier,which may due to keep the TJ closed and decrease expression of AQP4 protein.

ObjectiveTo observe the effect of Jiuqiang Naoliqing (JNQ) on the behavior of Kunming mice.MethodsSpontaneous movement, Morris Water Maze, Rotarod, anti caffeine test, sleeping time of pentobarbital sodium, subthreshold dose of pentobarbital sodium, and anti pentylene tetrazol test were adopted to evaluate the behavioral changes. ResultsCompared with the control group, the low dose of JNQ can increase spontaneous movement of the mice, the middle and high dose of JNQ can increase time on the rotating rods. JNQ can also increase sleeping time of pentobarbital sodium test and percent of falling asleep in subthreshold dose of pentobarbital sodium test, as well as antagonize caffeine's effect on mice. ConclusionJNQ can also do sedative and hypnotic effect on Kunming mice as well as improve their ability of balance and coordination.