OBJECTIVETo investigate the effect of extracellular regulating kinase (ERK) signaling pathway on the secretion of gamma-aminobutyric acid (GABA) in cultured rat hippocampal neurons induced by stromal cell derived factor-1 (SDF-1).

METHODSThe hippocampal neurons of newborn SD rats were cultured and identified in vitro; the phosphorylation level of ERK1/2 was examined by Western blot; ELISA was used to detect the effect of PD98059, a ERK1/2 specific blocker on GABA secretion of cultured hippocampal neurons and Western blot were adopted to measure the protein expression levels of glutamate decarboxylase (GAD65/67) and gamma aminobutyric acid transporter (GAT); after blocking ERK1/2 signaling pathway with PD98059; RT-PCR was used to detect the mRNA expression levels of GAT-1 and GAD65 after treated with PD98059.

RESULTSThe levels of ERKl/2 phosphorylation were increased significantly by SDF1 acting on hippocampal neurons, and CX-CR4 receptor blocker AMD3100, could inhibit SDF-1 induced ERK1/2 activation; SDF-1 could inhibit the secretion of GABA in cultured hippocampal neurons, and ERK1/2 specific inhibitor PD98059, could partly reverse the inhibition of GABA secretion by SDF-1. The effects of SDF-1 on cultured hippocampal neurons was to decrease the mRNA genesis of glutamic acid decarboxylase GAD65 and GABA transporter GAT-1, besides, ERK inhibitor PD98059 could effectively flip the effect of SDF-1. The results of Western blot showed that SDF-1 could inhibit the protein expression of GAT-1 and GAD65/67 in hippocampal neurons and the inhibition of GAT-1 and GAD65/67 protein expression could be partially restored by ERK1/2 blocker.

CONCLUSIONSDF-1 acts on the CXCR4 of hippocampal neurons in vitro, and inhibits the expression of GAD by activating the ERK1/2 signaling pathway, and this may represent one possible pathway of GABA secretion inhibition.

Animals ; Blotting, Western ; Cells, Cultured ; Chemokine CXCL12 ; pharmacology ; Flavonoids ; pharmacology ; Glutamate Decarboxylase ; metabolism ; Hippocampus ; cytology ; MAP Kinase Signaling System ; Neurons ; metabolism ; Phosphorylation ; RNA, Messenger ; Rats ; Rats, Sprague-Dawley ; Receptors, CXCR4 ; metabolism ; gamma-Aminobutyric Acid ; secretion

Objective To explore the mechanism of Niaochangshu capsule in the treatment of postmenopausal overactive bladder, through observing its influence on bladder weight and the expression of eNOS and AQP1 of ovariectomized female rats. Methods Female SD rats were divided into blank group, model group, Nilestriol group and Niaochangshu group. Rats were removed ovaries except the blank group. The treatment groups were given corresponding drugs, blank group and model group were given normal saline by gavage. After 4 weeks, the bladders' weight and thickness were detected, the expressions of eNOS and AQP1 in serum and bladder tissue were determined by ELISA, and NO by spectrophotometry. Results Ovariectomy resulted in decreased bladder weight, bladder mucosal and muscular atrophy, and opposite changes showed after given Niaochangshu. The expressions of eNOS and NO in bladder and serum were decreased significantly after ovariectomy, while increased by given Niaochangshu capsule or nylestriol (P<0.05), and there was significant difference between Niaochangshu group and Nilestriol group (P<0.05). The expression of AQP1 was decreased in the model group, and increased after given nylestriol or Niaochangshu capsule. While the expression of AQP1 in bladder had no significant difference among the four groups. Conclusion Niaochangshu capsule can reverse bladder mucosal and muscular atrophy caused by estrogen deficiency, and increase the content of eNOS in serum and bladder, thus play the role in the treatment of postmenopausal overactive bladder.

GJ-4 is crocin enrichments extracted from Gardenia jasminoides J. Ellis, and our previous studies have shown that GJ-4 significantly improved learning and memory impairment induced by Aβ in mice. Herein, a memory deficit model was developed by injecting okadaic acid (OA) into the lateral ventricle of mice, and the neuroprotection and underlying mechanism of GJ-4 on neuronal injury caused by Tau hyperphosphorylation were investigated. The Animal Care & Welfare Committee, Institute of Materia Medica, CAMS & PUMC has approved all procedures (No.00000318). GJ-4 at different doses was intragastric administration to mice for 16 days. Step-down test and Morris water maze test showed that GJ-4 could significantly improve OA-induced memory impairment in mice, and reduced the loss of Nissl bodies in the hippocampus of mice. GJ-4 could also decrease the phosphorylation level of Tau protein at Ser396, Thr231 and Ser404 via increasing protein phosphatase 2A (PP2A) activity and inhibiting glycogen synthase kinase-3β (GSK-3β) activity. Besides, further researches indicated that GJ-4 could inhibit the level of oxidative stress in the brain of OA mice, reduce neuronal apoptosis and inhibit the neuroinflammation mediated by activation of astrocytes in the hippocampus of mice, and eventually achieve its effects in improving learning and memory impairment in mice. According to these findings, we anticipated that GJ-4 might be a potential therapeutic drug for Alzheimer's disease.

Objective To investigate the effect of excessive fluoride,aluminum on Zn,Fe,Ca,Mg,Cuin rat blood.Methods Forty eight SD rats were randomly divided into 4 groups matched with their weights:control group,high aluminum group,high fluorine group and high fluorine-aluminum group.Aluminum content in their drinking water was 0,90,0,90 mg/L respectively.Fluorine content of their feed was 5.2,5.2,106.0,106.0 mg/kg and aluminum Was 6.8,6.8,19.7,19.7 mg/kg respectively.90 days later,the level of blood Zn,Fe,Ca,Mg, Cu Was detected by the atomic absorption spectrometry.Results Compared among these groups,Zn,Fe,Mg and Cu content of the whole blood had significant difierences(F=46.25,14.74,6.10,2.93,P<0.05),while Ca content of the whole blood did not significantly change(F=2.81.P>0.05).Factorial analysis showed that excessive intake of aluminum could significantly decreased Zn,Fe,Mg content of the blood(F=42.66,5.41,7.04,P<0.05)and excessive intake of fluorine could significantly decreased Zn,Fe,Mg,Cu content of the blood(F=64.50,37.90,9.75,6.74, P<0.05).The coexistence offluorine and Muminum had interaction to the level of Zn(F=31.59,P<0.05)and did not obviously interact with other elements(F=0.91,1.63,1.51.0.00,P>0.05).Compared with the control group [(131.30 ±13.86)μmol/L,(10.24 ±1.02),(1.71 ±0.19)mmol/L,(20.43 ±4.42)μmol/L],Zn content in the high aluminum group[(90.84±9.98)μmol/L]decreased significantly(P<0.05),so did Zn,Fe,Mg content in tlle high fluorine group[(85.85 ±10.92)μmol/L,(8.49 ±0.68),(1.52 ±0.13)mmol/L],the difference being statistically significant(P<0.05)0Zn,Fe,Mg,Cu content in the high fluorine-aluminum group,being(82.82 ±11.00)μmol/L, (8.16±0.45),(1.46±0.09)mmoL/L,(15.69±2.38)μmol/L,respectively,all decreased signitlcarIdy(P<0.05). Compared with the high aluminum group[(9.43±1.09)mmol/L],Fe content of the high fluorine aluminum group[(8.16±0.45)mmol/L]decreased significantly(P<0.05).Conclusions Excessive fluoride can cause blood zn, Fe,Mg,Cu decline,so can excessive aluminum.Combination of excessive fluofine and aiuminum has 8ignificant synergic effect on the level of Zn but have rio influence on Ca.

OBJECTIVETo examine serum IL-2 and IL-6 levels in BMS patients with or without depression and make clear the relationship between serum IL-2, IL-6 and mood disorder.

METHODSSerum IL-2 and IL-6 were examined in 48 BMS patients by means of ELISA. The Hamilton Depression Rating Scale (HDRS) was used to evaluate the depressive symptomatology.

RESULTSThere was no significant difference in serum IL-2 and IL-6 among BMS patients with or without depression. Mood disorder was not correlated to serum IL-2 and IL-6, but positively correlated to pain levels.

CONCLUSIONDepression status may not influence serum IL-2 and IL-6 levels significantly, but it has a relationship with BMS. The HDRS can be used to determine depression status in BMS patients in order to help clinical treatment.

Adult ; Aged ; Aged, 80 and over ; Burning Mouth Syndrome ; blood ; psychology ; Depressive Disorder ; blood ; psychology ; Enzyme-Linked Immunosorbent Assay ; Female ; Humans ; Interleukin-2 ; blood ; Interleukin-6 ; blood ; Male ; Middle Aged ; Pain Measurement ; Psychiatric Status Rating Scales

Alkaloids ; pharmacology ; Animals ; Liver Neoplasms, Experimental ; enzymology ; prevention & control ; Quinolizines ; pharmacology ; Rats ; Selenium ; pharmacology ; Telomerase ; metabolism ; Yeast, Dried ; pharmacology

OBJECTIVETo evaluate the benzene exposure level and cytopenia among the benzene exposed workers in Shanghai, China and to analyze the influential factors for the health of benzene-exposed workers.

METHODSA total of 3314 benzene-exposed workers, who were from 85 benzene-related enterprises selected by stratified random sampling based on enterprise sizes and industries, were included in the study. The time-weighted average (TWA) concentration of benzene in each workshop was measured by individual sampling and fixed point sampling, and the benzene exposure level in workshop was evaluated accordingly. The occupational health examination results and health status of benzene-exposed workers were collected.

RESULTSThe median of TW A concentrations of benzene was 0.3 mg/m3. The TWA concentrations measured at 7 ( 1.4%) of the 504 sampling points were above the safety limit. Of the 7 points, 3 were from large enterprises, 2 from medium enterprises, and 2 from small enterprises; 3 were from shipbuilding industry, 1 from chemical industry, and 3 from light industry. Of the 3314 benzene-exposed workers, 451 ( 13.6%) had cytopenia, including 339 males ( 339/2548, 13.3%) and 112 females ( 112/766, 14.6% ). There were significant differences in the incidence rates of leukopenia and neutropenia among the benzene-exposed workers of different sexes and ages (P<0.05); there were significant differences in the incidence rate of cytopenia among the benzene-exposed workers of different ages and working years ( P<0.05 ); there were significant differences in the incidence of neutropenia among the benzene exposed workers of different working years ( P<0.05).

CONCLUSIONMonitoring and intervention measures should be enhanced to protect the benzene-exposed workers in the large enterprises in shipbuilding industry and medium and private enterprises in chemical industry from occupational hazards.

Adolescent ; Adult ; Benzene ; toxicity ; China ; epidemiology ; Female ; Humans ; Male ; Middle Aged ; Occupational Exposure ; Pancytopenia ; chemically induced ; epidemiology ; Young Adult

To study the effects of recombinant human tumor necrosis factor-alpha (rhTNF-alpha) on HL-60 cells in vitro and in vivo, MTT and colony forming assay were used to examine the effects of rhTNF-alpha on proliferation of HL-60 cells; AO/EB (acridine orange-ethidium bromide) staining, Annexin-V flow cytometry analysis and TUNEL assay were used to detect apoptotic cells. The effect of rhTNF-alpha on xenograft growth of HL-60 cells was evaluated by tumor inhibition rate, histology, ultrastructure and TUNEL assay. The results showed that rhTNF-alpha inhibited the proliferation of HL-60 cells in a dose-dependent manner. Staining of cells with AO/EB revealed that rhTNF-alpha induced nuclear chromatin condensation and fragmentation. Positive Annexin V-FITC on cell membrane showed that rhTNF-alpha induced apoptosis of HL-60 cells in a dose-dependent manner. TUNEL assay showed that the apoptotic percentage of HL-60 cells reached 37.5% when incubated with 3200 U/ml rhTNF-alpha for 48 hours. In vivo rhTNF-alpha inhibited xenograft growth of HL-60 cells with the highest inhibition rate of 60.33%. Pathologically it was found that there were necrotic areas in the tumors of groups treated with rhTNF-alpha. There were more apoptotic cells in treatment groups than in that control group by transmission electron microscopy (TEM) and TUNEL assay. It is concluded that rhTNF-alpha is able to inhibit the proliferation of HL-60 cells and to induce apoptosis of HL-60 cells in vitro and in vivo.
Animals ; Antineoplastic Agents ; pharmacology ; Apoptosis ; drug effects ; Cell Proliferation ; drug effects ; Dose-Response Relationship, Drug ; HL-60 Cells ; Humans ; Leukemia, Promyelocytic, Acute ; drug therapy ; Mice ; Mice, Inbred BALB C ; Mice, Nude ; Neoplasm Transplantation ; Recombinant Proteins ; pharmacology ; Tumor Necrosis Factor-alpha ; pharmacology

OBJECTIVETo observe the millimeter wave therapy responses in patients with burning mouth syndrome.

METHODSEighty patients were randomized divided into 4 groups. The first group was treated with both millimeter wave irradiation and routine medication, the second group with millimeter wave irradiation, the third with pretending millimeter wave irradiation and routine medication and the fourth with routine medication. Pain, extravasated blood level and autonomic nerve system condition were double-blindly evaluated either before or after the treatment.

RESULTSStatistically significant difference (P < 0.05) was found as the degree of pain was compared before and after treatment of all the 4 groups. The first and second group, which were affected by the millimeter wave irradiation, had obvious improvements in the extravasated blood level and autonomic nerve system condition (P < 0.05). When the 4 groups were compared with each other, there were significant differences (P < 0.05) between the first and the fourth groups, and the second and the fourth groups regarding the reduction of pain. According to extravasated blood level, significant differences (P < 0.05) were found in the first and third or fourth groups, the second and third or fourth groups.

CONCLUSIONSThe irradiation of holographic point by millimeter wave can improve the patients' pain, extravasated blood level and autonomic nerve system condition. It might provide a new treatment method for burning mouth syndrome.

Acupuncture Points ; Burning Mouth Syndrome ; therapy ; Humans ; Microwaves ; therapeutic use ; Treatment Outcome

BACKGROUNDPrenatal hyperglycaemia may increase metabolic syndrome susceptibility of the offspring. An underlying component of the development of these morbidities is hepatic gluconeogenic molecular dysfunction. We hypothesized that maternal hyperglycaemia will influence her offsprings hepatic peroxisome proliferator-activated receptor coactivator-1α (PGC-1α) expression, a key regulator of glucose production in hepatocytes.

METHODWe established maternal hyperglycaemia by streptozotocin injection to induce the maternal hyperglycaemic Wistar rat model. Offspring from the severe hyperglycemia group (SDO) and control group (CO) were monitored until 180 days after birth. Blood pressure, lipid metabolism indicators and insulin resistance (IR) were measured. Hepatic PGC-1α expression was analyzed by reverse transcription polymerase chain reaction and Western blotting. mRNA expression of two key enzymes in gluconeogenesis, glucose-6-phosphatase (G-6-Pase) and phosphoenolpyruvate carboxykinase (PEPCK), were analyzed and compared.

RESULTSIn the SDO group, PGC-1α expression at protein and mRNA levels were increased, so were expression of G-6-Pase and PEPCK (P < 0.05). The above effects were seen prior to the onset of IR.

CONCLUSIONThe hepatic gluconeogenic molecular dysfunction may contribute to the metabolic morbidities experienced by this population.

Animals ; Female ; Hyperglycemia ; chemically induced ; physiopathology ; Insulin Resistance ; physiology ; Liver ; metabolism ; Male ; Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha ; Peroxisome Proliferator-Activated Receptors ; metabolism ; Pregnancy ; Prenatal Exposure Delayed Effects ; RNA-Binding Proteins ; Rats ; Rats, Wistar ; Streptozocin ; toxicity ; Transcription Factors