Objective To investigate the effectiveness and safety of combined heparin and acutobin in the treatment of acute inferior vena cava thrombus in rabbits. Methods The inferior vena cava thrombus model was established in 72 rabbits and they were randomly divided into three groups; heparin group(A) , group for combination of urokinase and heparin (B), group for combination of acutobin and heparin (C) ,each group including 24 rabbits. Drugs were administrated 3 days after thrombosis. Coagulation indexes were tested to assess their safety, and Doppler ultrasound was used to assess their effectiveness, on day 3, day 7, and day 10. Results The prolongation of prothrombin time ( PT) in group C was shorter than that in group B( P < 0. 05 ) , the fibrinogen ( FBG) value in group C was lower than that in group B (P < 0. 05 ) , the prolongation of PT in group B and group C was longer than that in group A (P < 0. 01), the FBG value of group B and C were higher than that in group A ( P < 0. 01 ), D-dimer ( D-D) value in group B and C gradually returned to normal range. There was no difference between the two groups (P > 0. 05). The thrombolytic effect in group B and C were better than that in group A, statistical difference was reached between groups B and A (P <0. 01), and the difference was statistically significant between groups C and A 10 days after administration (P < 0. 01). Thrombolytic effect was not different statistically between groups B and C (P > 0. 05). Conclusion Acutobin combined with heparin in the treatment of acute inferior vena cava thrombus in rabbits was effective and safe.

Objective To evaluate the changes in the expression of acetylated histone H3 (Ac-H3) and deacetylase silent information regulator 1 (SIRT1) in dorsal root ganglions in a rat model of negative phenotype neuropathic pain.Methods Forty-eight male Sprague-Dawley rats,weighing 250-300 g,were randomly divided into 2 groups (n =24 each):sham operation group (group S) and C-fiber dysfunction group (group CFD).The rats were anesthetized with 10％ chloral hydrate 3 ml/kg.C-fiber dysfunction was induced by exposing sciatic nerve to 8％ capsaicin for 30 min in group CFD.The thermal withdrawal latency (TWL) and mechanical withdrawal threshold (MWT) were measured before and on 1,3,7 and 14 days after CFD.Six rats were then sacrificed at each time and the lumbar segments (L5) of the dorsal root ganglions were removed for detection of SIRT1 mRNA expression (by RT-PCR) and Ac-H3 and SIRT1 protein expression (by Western blot).Results Compared with group S,TWL was significantly increased at 1,3,7 and 14 days after CFD,SIRT1 mRNA and protein expression was up-regulated and Ac-H3 expression was down-regulated at 3,7 and 14 days after CFD (P ＜ 0.05),while no significant change was found in MWT at each time point in group CFD (P ＞ 0.05).Conclusion The mechanism of negative phenotype neuropathic pain is related to up-regulation of deacetylase SIRT1 expression and decreased acetylation of histone H3 in rat dorsal root ganglions.

Objective To observe the effect of δ-opioid receptor on proliferation and migration of human epidermal stem cells (hESCs) in vitro so as to offer treatment theory for skin injury.Methods hESCs from fresh foreskin tissues of normal young volunteers were isolated and cultured by enzyme digestion and differential adherence technique.Immunofluorescent staining was used to determine expression of integrin β1 and cytokeratin 19 (CK19) and flow cytometry was used for cell count.Second generation of cells were cultured for 5 consecutive days with keratinocyte serum-free medium (K-SFM) supplemented with 1 nmol/L (D-Ala2,K-Leu5)-enkephalin in Group A,with K-SFM supplemented with 1 nmol/L naltrindole and 1 nmol/L (D-Ala2,K-Leu5)-enkephalin in Group B,and with isolated K-SFM in Group C.Cellular division and proliferation were detected by MTT method.An in vitro 100 μm scratch-wound model was created on the confluent monolayer cells at 24 hours of incubation.Cells migrating from the wound margin were determined by inverted phase contrast microscope at 24,48,72,and 96 hours after wound formation,while wound closure rate was calculated at 72 hours.Results Primary cultured hESCs presented cobblestone-like shape after adherence growth,Immunofluorescence staining showed positive results for integrin β1 and CK19 and cell purity reached 95.6％.Moreover,MTT findings revealed proliferation of hESCs enhanced significantly in Group A,but lowered in Group B as compared to Group C (P ＜ 0.05).hESCs migrated from the wound margin in all groups at 24 hours.However,more migrated cells were seen in Group A than in Group C and less in Group B than in Group C.Rate of wound closure was (89.5 ±0.7)％ in Group A,(76.1 ±0.3)％ in Group B,and (81.1 ±0.6)％ in Group C at 72 hours,indicating significant differences among groups (P ＜ 0.05).Conclusion Activation of δ-opioid receptor promotes the proliferation and migration of hESCs in vitro and may be implicated in wound healing.

OBJECTIVETo evaluate efficacies of three commonly used oral drugs including Berbamine Hydrochloride Tablet (B), Qijiao Shengbai Capsule (Q), and Leucogen Tablet (L) (by single drug, two drugs or three drugs) combined with granulocyte colony-stimulating factor (G-CSF) for treat ment of chemotherapy related leukocytopenia in mice.

METHODSTotally 156 Kunming male mice were divided into the normal control group (A, n=24), the model group (B, n=24), the G-CSF group (C, n =24), the G-CSF+Q group (D, n=12), G-CSF+ B (E, n=12), the G-CSF+L group (F, n=12), the G-CSF + Q + B group (G, n=12), the G-CSF + Q + L group (H, n=12), the G-CSF + L + B group (I, n=12), and the G-CSF + L + Q + B (J, n=12). Mouse models of chemotherapy related leukocytopenia were established by intraperitoneal injection of cyclophosphamide (CTX). A G-CSF group was set up as a positive control. Mice were treated by a single oral drug, a single oral drug combined with G-CSF, and two or three drugs combined with G-CSF respectively, and the death rate calculated. Hemocytes [such as white blood cells (WBC) and its classification, red blood cells (RBC), platelet (PLT), hemoglobin (Hb)] were calculated by hematology analyzer. Mice were anatomized and important organs weighed. Organ indices were calculated.

RESULTSThere was no statistical difference in the mortality rate among all groups (P > 0.05). Compared with Group B, WBC was elevated in all other groups (P < 0.01). WBC and PLT were elevated most in Group J, Hb and RBC were also increased at the same time (P < 0.05, P < 0. 01). Compared with Group B, RBC increased in Group E, F, G, I, and J (P < 0.01); Hb obviously increased in Group C, E, F, H, I, and J (P<0.01). Compared with Group B and D, the promotion of erythroid hematopoiesis by G-CSF could be elevated in any group contained drug B and L (P < 0.05, P < 0.01). The spleen index of model mice could be significantly improved in Group C, D, and G (P < 0.01). The thymus index of model mice could be significantly improved in Group H (P < 0.05).

CONCLUSIONSThe best scheme to treat mice with chemotherapy related leukopenia or decreased three blood series was to administrate three commonly oral drugs combined with G-CSF. Authors speculated that G-CSF and Q might have a certain effect on CTX induced immune inhibition.

Administration, Oral ; Animals ; Blood Platelets ; Cyclophosphamide ; Drug-Related Side Effects and Adverse Reactions ; drug therapy ; Drugs, Chinese Herbal ; pharmacology ; Erythrocyte Count ; Granulocyte Colony-Stimulating Factor ; metabolism ; Hematopoiesis ; Hemoglobins ; Leukocyte Count ; Leukocytes ; Leukopenia ; chemically induced ; drug therapy ; Male ; Mice ; Pharmaceutical Preparations

Objective To study the mechanism of killing and apoptosis-inducing effects of Capparis spinosa alkaloid (CSA) on human hepatocarcinoma cell line HepG2. Methods The killing effect of CSA on human hepatocarcinoma cell line HepG2 was studied by MTT method. Morphological observation of HepG2 cells was carried out by fluorescence microscope. Results The CSA had obvious cytotoxicity on the HepG2 in a dose-dependent manner and its IC50 value was 142.82 ?g/mL. The HepG2 cells showed the characteristic morphologic changes of apoptosis by the function of CSA and the apoptosis percentage is higher than that of the natural one. The progress of cells cycle from S phase to G2 phase had been blocked by CSA. The intracellular Ca2+ level had been increased by the function of CSA, which was positively related with drug concentration. Conclusion CSA has obviously killing and apoptosis-inducing effects on human hepatocarcinoma cell line HepG2 and calcium overload might also be invovled in these events.

Objective To establish the animal model for the study of children with moderate blood lead levels in young rabbits,for the study of the ideal therapy for moderate lead poisoning in children.Methods Sixteen 45-day-old male New Zealand rabbits were randomly divided into control and lead-exposed group,8 in each group.Rabbits in the lead-exposed group were treated with 5 mg/(kg?d)lead acetate in their forage for 6 weeks to establish moderate lead poisoning animal model.The blood lead levels(BLLs)were determined by atomic absorption spectrometer(AAS),and the urine lead levels and the lead concentrations of tissue and organ were determined by inductively coupled plasma-mass spectrometry(ICP-MS).Histopathology in tissue and organ was observed under the light microscope.Results The BLLs and the urine lead levels in lead-exposed group step up rapidly in primal weeks,then retained at a steady levels.The BLLs exhibited moderate level BLLs during the lead exposure period.Compared with control group,the body weight gain,testis and hippocampus wet coefficient of the lead-exposed group significantly decreased(P_a

OBJECTIVETo observe the effect of paiqian chewing tablet (PQCT) on lead discharging and health in children.

METHODSAdopting self-control and inter-group control method, 94 children with blood lead level exceeding 100 microg/L were randomly divided into the observed group and the control group. The observation period for both groups was 30 days.

RESULTSAt the 20th and 30th day of treatment, the urinary lead output in the observed group was significantly higher than that in the control group (P < 0.05, P < 0.01), and showed significant difference as compared with that before treatment (P < 0.05). Besides, the total amount of urinary lead discharging in the observed group was significantly more than that in the control group (P < 0.05).

CONCLUSIONPQCT has markedly lead discharging improvement action with no influence on urinary calcium and zinc excretion. As all the routine indexes of blood and urine ranged within the normal extent, it demonstrated that PQCT was harmless to the health of observed individual.

Child ; Double-Blind Method ; Drugs, Chinese Herbal ; therapeutic use ; Female ; Humans ; Lead ; blood ; urine ; Lead Poisoning ; drug therapy ; Male ; Phytotherapy ; Tablets

OBJECTIVETo investigate the apoptosis effect of isothiocyanates (ITCS) on human liver cancer cells HepG-2, and its mechanism.

METHODHepG-2 cells were treated with different concentrations of ITCS. MTT assay was used to evaluate the influence of ITCS on cell proliferation. Flow cytometry was used to test ROS levels, intracellular mitochondrial transmembrane potential (deltapsim) , and hypodiploid apoptosis peak in HepG-2 cells.

RESULTITCS obviously inhibited proliferation of HepG-2 cells. When treated with 15, 30, 60, 120, 240 microg x mL(-1) of ITCS for 24 h, ROS levels were (23.1+/-1. 8)%, (53.3+/-3.3)%, (57.9+/-2.0)%, (79.9+/-3.4)%, (93.4+/-2. 6)% respectively; and deltapsim were (94.8+/-5.5)%, (91.8+/-5.4)%, (66.0+/-5.6)%, (65. 5+/-6.6)% and (44.3+/-2.7)% respectively; when treated with 60, 120, 240 microg x mL(-1) of ITCS for 48 h, cell apoptotic rates were (16.6+/-2.8)%, (21.9+/-4.4) % and (70.2+/-5.3) % respectively.

CONCLUSIONITCS generates ROS in gastric cancer HepG-2 cells, which causes mitochondrial membrane permeabilization and deltapsim decrease, therefore, leads to apoptosis of HepG-2 cells.

Antineoplastic Agents, Phytogenic ; isolation & purification ; pharmacology ; Apoptosis ; drug effects ; Brassica ; chemistry ; Cell Line, Tumor ; Cell Proliferation ; drug effects ; Humans ; Isothiocyanates ; isolation & purification ; pharmacology ; Liver Neoplasms ; metabolism ; pathology ; Membrane Potential, Mitochondrial ; drug effects ; Mitochondria, Liver ; drug effects ; physiology ; Plants, Medicinal ; chemistry ; Reactive Oxygen Species ; metabolism

OBJECTIVETo investigate the role of T cell and its subsets in the induction of insulitis and type 1 diabetes mellitus (T1DM) in BALB/c mice.

METHODSAutoimmune diabetes mellitus was developed by intraperitoneal injection of 40 mg/kg streptozotocin (STZ) daily for 5 consecutive days in BALB/c mice as sources of donor cells. Spleen cells from diabetic mice were then cultured for 7 days in the stimulation of interleukin-2 (IL-2) to harvest diabetogenic T cells, which were subsequently transferred into normal BALB/c mice recipients. MTT, ELISA, and HE staining were used to analyze the lymphocyte proliferation, cytokine (IL-2, interferon-gamma, IL-4, and IL-10) levels, and pathological changes in pancreatic islets.

RESULTSAs few as 3 x 10(6) diabetogenic T cells successfully induced diabetes mellitus in recipients pretreated with STZ twice, whereas transfer of equal amount of normal splenocytes, T cell-depleted diabetogenic splenocytes, or diabetogenic CD4+ T cells alone in recipients receiving STZ twice pretreatment was proved not to induce diabetes mellitus either. A markedly increased lymphocyte proliferation, high levels of interferon-gamma and IL-2 in the supernatants of diabetogenic T cells were observed. In addition, a markedly enhanced lymphocyte proliferation, a high level of interferon-gamma secretion in serum, and numerous lymphocytes infiltration in pancreatic islets were detected in the diabetic mice induced by diabetogenic T cells transfer.

CONCLUSIONSA novel T1DM murine model is established in STZ-pretreated BALB/c mice by adoptive transfer of diabetogenic T cells. CD4+ T cells with interferon-gamma may promote the onset of diabetes mellitus.

Animals ; Blood Glucose ; metabolism ; Cytokines ; immunology ; Diabetes Mellitus, Experimental ; metabolism ; pathology ; Diabetes Mellitus, Type 1 ; immunology ; pathology ; Disease Models, Animal ; Islets of Langerhans ; cytology ; metabolism ; pathology ; Male ; Mice ; Mice, Inbred BALB C ; T-Lymphocytes ; cytology ; immunology

OBJECTIVETo establish a rabbit model of abdominal compartment syndrome (ACS) and evaluate the impact of ACS on cardiovascular and respiratory functions and blood electrolyte levels in rabbits.

METHODSTwenty-four New Zealand rabbits were randomly allocated into 4 equal groups, namely the normal control group, ACS(5>\) group [intra-abdominal pressure (IAP)=5 mmHg], ACS(10) group (IAP=10 mmHg) and ACS(20) group (IAP=20 mmHg). ACS model was established by intra- abdominal bleeding (IAB) with intra-abdominal hypertension (IAH). All the data were recorded 1 h after inducing IAH including cardiovascular parameters (LVSP, LVEDP, ∓dp/dt max, SP, DP, HR, CVP), respiratory function (RR, PaO(2), PaCO(2), [HCO(3)(-)]), blood pH, and electrolyte level ([K(+)]).

RESULTSCompared with those in the normal control group, ACS20 group showed significantly decreased LVSP, LVEDP, ∓dp/dt max, SP, DP, HR, RR, PaO(2), [HCO(3)(-)], and blood pH but increased CVP, PaCO(2), and K(+) (P<0.05). In ACS(10) group, all the parameters except for RR and PaO(2) showed similar changes as seen in ACS(20) group (P<0.05) but with lower amplitudes of variations. In ACS(5) group, only LVSP and HR were reduced remarkably (P<0.05) while the other parameters showed no significant variations.

CONCLUSIONIAB plus IAH may cause damage to the cardiovascular and respiratory functions and lead to ACS in rabbits.

Abdominal Cavity ; physiopathology ; Animals ; Blood Gas Analysis ; Disease Models, Animal ; Intra-Abdominal Hypertension ; blood ; physiopathology ; Rabbits ; Respiratory System ; physiopathology ; Ventricular Function, Left