OBJECTIVETo investigate anticancer effects of 5-fluorouracil (5-FU) combined with CL, extract of Rosa roxburghii Tratt on human endometrial adenocarcinoma cell line (JEC).

METHODSJEC cells cultured in vitro in the logarithmic growth phase were seeded in the culture plate and divided into the control group (RPMI 1640), the positive group (10(-4) mol/L 5-FU), the CL groups (at the dose of 0.01, 0.1, 1, 10, and 100 microg/mL), and the CL (0.01, 0.1, 1, 10, and 100 microg/mL) combined with 5-FU groups. Effects of 5-FU combined with CL on JEC cell growth were drawn and measured by MTT and growth curves. Effects of CL combined with 5-FU on the JEC cell differentiation was analyzed by detecting the reduction capability of nitrobenzene thiocyanate (NBT) and lactate dehydrogenase (LDH) contents in the cultured medium. Effects of CL combined with 5-FU on the JEC cell apoptosis and cell proliferation cycle were detected by acridine orange (AO)/ethidium bromide (EB) fluorescent staining and flow cytometry (FCM).

RESULTSThe proliferation inhibitory effect of CL combined with 5-FU on JEC cells was enhanced when compared with that of CL or 5-FU alone (P<0.05). The percentages of NBT positive JEC cells and apoptotic JEC cells increased in the 5-FU combined with CL groups when compared with 5-FU group or the CL group alone (P<0.05). The LDH concentration of the JEC cell culture supernate decreased in 5-FU combined with CL groups (P<0.05). Furthermore, the percentage of G0-G1 phase JEC cells treated by 5-FU combined with CL was higher than that of 5-FU or CL alone (P<0.05).

CONCLUSIONCL could enhance anticancer effects of 5-FU. Its mechanisms might be correlated with reinforcing the cytotoxicity of 5-FU, inducing cell differentiation and apoptosis, and inhibiting cell proliferation and division.

Adenocarcinoma ; pathology ; Cell Differentiation ; drug effects ; Cell Line, Tumor ; Cell Proliferation ; drug effects ; Endometrial Neoplasms ; pathology ; Female ; Fluorouracil ; pharmacology ; Herb-Drug Interactions ; Humans ; Plant Extracts ; pharmacology ; Rosa ; chemistry

Objective To investigate the capability of empathy for pain in migraineurs without aura.Methods Thirty migraineurs without aura and thirty matched healthy controls were recruited.Picturecued Empathy for pain paradigm was used to compare the capability of empathy in the migraine group with that in the control group.Results Compared with the control group,the migraine group had diminished ability to discriminate painful from nonpainful pictures,and the discrimination accuracy was significantly reduced ((2.55±0.61) vs (2.88±0.38);t=-2.505,P=0.01).In the task laterality,there was no difference in discrimination accuracy between two groups(P＞0.05).The rating scores of patients were evidently smaller than those of control group ((3.01±0.52) vs (3.37±0.47);t=-2.827,P=0.006).Pearson correlation analysis showed that the age of migraineurs was negatively correlated with the discrimination accuracy(r=-0.393,P =0.031),and there was no correlation between migraineurs' educational years,disease course,severity,Mini-mental State Examination,Hamilton Anxiety Scale,Hamilton Depression Scale,Verbal Fluency Test,Stroop Test and the idex of empathy for pain (all P＞0.05).Conclusion Migraineurs without aura have deficiency in the capability of empathy for pain.

OBJECTIVETo study the effect of electroacupuncture on nitric oxide synthase (NOS) in rats with cerebral ischemia-reperfusion injury.

METHODSFocal cerebral ischemia-reperfusion model was established using modified intravascular suture technique. The NO content in the brain tissue was detected by nitrite reduction and the expressions of nNOS and iNOS were detected by immunohistochemistry. Eighty rats in this experiment were divided into the normal group, the cerebral ischemia-reperfusion injury model group (as the model group), the cerebral ischemia-reperfusion injury + electroacupuncture group (as the acupuncture group), and the cerebral ischemia-reperfusion injury + phosphatidylinositol 3 kinase (PI3-K) inhibitor group (as the inhibitor group). Each group consisted of twenty rats. Five microL PI3-K inhibitor LY294002 (400 microL) was slowly injected at the lateral cerebral ventricle of rats in the inhibitor group at a constant speed using microinjector according to Konig Klippel atlas of the stereotaxis instrument. Shuigou (DU26) and Chengjiang (RN24) were selected to determine levels of NO and NOS.

RESULTSAfter 24-h ischemia-reperfusion, the NO levels of the hippocampus and the cerebral cortex increased abnormally, and the expressions of nNOS and iNOS increased, showing significant difference when compared with those of the normal group (P<0.05). By electroacupuncture at Shuigou (DU26) and Chengjiang (RN24), the ischemic cerebral ischemia-reperfusion injury neuron loss was inhibited. Meanwhile, the high levels of NO, nNOS and iNOS in the cerebral cortex and the hippocampus were significantly inhibited (P<0.05). The abnormally increased expressions of nNOS and iNOS were reversed, showing significant difference when compared with the model group (P<0.05). But when compared with the normal group, there was no significant difference (P>0.05). The effects of electroacupuncture reversed the abnormally increased NO levels of the hippocampus and the cerebral cortex and expressions of nNOS and iNOS after LY294002 oppressed anti-PI3K to block the TrkA acceptor circuit. The NO levels of the hippocampus and the cerebral cortex and expressions of nNOS and iNOS increased again, showing significant difference when compared with the acupuncture group (P<0.05).

CONCLUSIONSAcupuncture fought against cerebral ischemia and reperfusion in the loss of neurons, at the same time, the abnormal regulation of NOS had reverse effect partly through TrkA/PI3K mediated signal transduction pathway.

Animals ; Brain Ischemia ; metabolism ; Electroacupuncture ; Nitric Oxide ; metabolism ; Nitric Oxide Synthase Type I ; metabolism ; Nitric Oxide Synthase Type II ; metabolism ; Rats ; Rats, Sprague-Dawley ; Reperfusion Injury ; metabolism ; Signal Transduction

Child ; Histiocytosis, Sinus ; diagnosis ; drug therapy ; Humans ; Lymphatic Diseases ; diagnosis ; drug therapy ; Male

OBJECTIVETo investigate anticancer effects and potential mechanisms of CL, extract of Rosa roxburghii.

METHODIn vitro anticancer effect was observed in Ehrlich's ascites carcinoma (EAC) mice model. Cell toxicity of CL on human endometrial adenocarcinoma cell line JEC (JEC) cells was measured by MTT reduction test and growth curves drawing by trypan blue dye exclusion method. Lactate dehydrogenase (LDH) concentration of cultured medium was detected by auto-biochemistry-meter. Cell differentiation was showed by detection of NBT reduction ability. Apoptosis was showed by AO/EB fluorescent staining and flow cytometer detection. Cell proliferation cycle was detected by flow cytometer.

RESULTComparing with the negative group, life span of EAC mice treated with CL was prolonged (P <0.05), and thymus index and spleen index of them were raised (P <0.05). The inhibitory effect of CL on JEC cells was in concentration-and time-dependent manner. IC50 of CL on JEC cells was 0.05 microg mL(-1) in 96 hours. Growth curves showed right-shift with CL concentration increasing. The number of NBT positive JEC cells increased and the LDH concentration of cultured medium declined with CL increasing. Apoptosis of JEC cells with CL treated was induced in concentration-dependent manner, apoptotic percentage of CL 10 microg mL(-1) on JEC cells was 25.59% in 24 hours. CL arrested JEC cells in G2-M phase (P <0.05).

CONCLUSIONCL has certainly anticancer effects in vivo and in vitro. Anticancer effect of CL in vivo was in relation to enhancing immune function of EAC mice; anticancer mechanisms of CL on JEC cells may be its direct cytotoxic effect, inducing cell apoptosis and inhibiting cell segmentation.

Adenocarcinoma ; metabolism ; pathology ; Animals ; Antineoplastic Agents, Phytogenic ; administration & dosage ; pharmacology ; Apoptosis ; drug effects ; Carcinoma, Ehrlich Tumor ; pathology ; Cell Cycle ; drug effects ; Cell Line, Tumor ; Dose-Response Relationship, Drug ; Drugs, Chinese Herbal ; administration & dosage ; pharmacology ; Endometrial Neoplasms ; metabolism ; pathology ; Female ; Humans ; L-Lactate Dehydrogenase ; metabolism ; Mice ; Plants, Medicinal ; chemistry ; Random Allocation ; Rosa ; chemistry

The chemical investigation on Ganoderma philippii led to the isolation of sixteen compounds by silica gel and Sephadex LH-20 column chromatography. On the basis of spectroscopic data analyses, their structures were elucidated as 2, 5-dihydroxyacetophenone (1), methyl gentisate (2), (S) -dimethyl malate (3), muurola-4, 10 (14) -dien-11beta-ol (4), dihydroepicubenol (5), 5-hydroxymethylfuran carboxaldehyde (6), ergosta-7, 22E-dien-3beta-ol (7), ergosta-7, 22E-dien-3-one (8), ergosta-7, 22E-diene-2beta, 3alpha, 9alpha-triol (9), 6/beta-methoxyergo-sta-7, 22E-dien-3beta, 5alpha-diol (10), ergosta-4, 6, 8(14), 22E-tetraen-3-one (11), ergosta4, 6, 8-(14), 22E-etetraen-3beta-ol (12), 5alpha, 8alpha-epidioxy-ergosta-6, 22E-dien-3beta-ol (13), 7alpha-methoxy-5alpha, 6alpha-epoxyergosta-8-(14), 22E-dien-3beta-ol (14), ergosta-8, 22E-diene-3beta, 5alpha, 6beta, 7alpha-tetraol (15), and ergosta-5, 23-dien-3beta-ol, acetate (16). All the compounds were obtained from this fungus for the first time, and compounds 4 and 5 were isolated from the Ganoderma genus for the first time.
Ganoderma ; chemistry ; Medicine, Chinese Traditional ; Organic Chemicals ; analysis ; isolation & purification

Objective The invasion and metastasis of colon cancer often leads to treatment failure and mortality in patients . Our research is to investigate the influence of FoxM 1 to malignant human colon cancer line . Methods In two human colon cancer lines, the protein and mRNA expression levels of FoxM 1 were analyzed with the application of RT-PCR and Western blot , from which high-expressed HT-29 and low-expressed HCT-116 were determined.The expression of FoxM1 was down-regulated by RNA interfering in HT-29 and up-regulated by constructing overexpression transgenic line in HCT-116.The proliferation of the above cells was assayed by healing method;while the metastasis and invasion ability were examined by Transwell chamber assay . Results Two colon cancer lines were selected with high-expression or low-expression of FoxM1 separately named HT-29 and HCT-116.Application of PEX-2-FoxM1 raised after HCT-116 cells express FoxM1, cell scratches in HCT-116 experimetal group ([70.92 ±1.48]%) compared with HCT-116 control group([16.92 ±4.05]%)and HCT-116 blank control group([16.66 ±2.63]%) will markedly enhance its capabil-ity of healing (P<0.05), Transwell Chambers in membrane cells in HCT-116 experimetal group (186.0 ±6.8) compared with HCT-116 control group(42.0 ±2.0) and HCT-116 blank control grou (37.0 ± 2.2)was increased (P<0.05).On the other hand, the applied pG-PH-shFoxM1 can reduce FoxM1 expression in HT-29 cell, cell scrat-ches healing ability in HT-29 experimetal group ( [ 10 .37 ± 3.86]%) compared with HT-29 control group([34.63 ±2.35]%)and HT-29 blank control group([67.36 ±2.61]%) decreased significantly (P<0.05), Transwell Chambers in membrane cells in HT-29 experimetal group (53.0 ±1.8)compared with HT-29 control group(95.0 ±2.2)and HT-29 blank control grou(118.0 ±4.0) was also reduced (P<0.05). Conclusion The expression of FoxM1 is in close relation to the invasion and metastasis of CRC .The fact that the siRNA interfering FoxM1 could effectively inhibit the proliferation, metastasis and invasion, suggesting FoxM1 could po-tentially be a new molecular target for inhibiting the proliferation of human colon cancer line .

OBJECTIVETo investigate the therapeutic effects of Angelica sinensis polysaccharide-iron complex (APIC) on rats with iron deficiency anemia (IDA).

METHODSThe IDA rat model was established by adopting low-iron forage with a small amount of regular bloodletting. The rats were randomly divided into a model group, three AIPC groups (high, middle, and low dosage), an Angelica sinensis polysaccharide (ASP) group, a mixture group (ASP+FeCl(3)) and a positive control group (Niferex). Changes in hemoglobin (Hb), red blood cell count (RBC), hematocrit (HCT) and iron content of whole blood were observed.

RESULTSThere was a significant difference before and after administration in all treated groups and all indices were restored to near-normal levels in the APIC groups and the positive control group. There was a significant difference among the changes of the indices in all the APIC groups and those of the model group but not between those of the APIC groups and the positive control group. However, the recovery of the indices in the APIC groups was superior to that in the positive control group.

CONCLUSIONAPIC not only has a superior therapeutic effect on IDA, but also has the effect of the ASP on supplementing blood and activating blood circulation. Hence, it may be used as a new iron-supplementing agent with a double therapeutic efficacy on blood supplementation for the treatment of IDA.

Anemia, Iron-Deficiency ; drug therapy ; Animals ; Dose-Response Relationship, Drug ; Drugs, Chinese Herbal ; chemistry ; therapeutic use ; Female ; Iron ; blood ; chemistry ; therapeutic use ; Male ; Polysaccharides ; chemistry ; therapeutic use ; Rats ; Rats, Sprague-Dawley

OBJECTIVETo evaluate the prognostic implication of the killer-immunoglobulin like receptor (KIR) ligand mismatch in HLA mismatched hematopoietic stem cell transplantation (HSCT).

METHODSNinety-four leukemia patients undergoing unmanipulated HLA-mismatched/haploidentical blood and marrow HSCT enrolled this study.

RESULTSMultivariate analysis showed that both KIR ligand mismatch (HR 2.833, CI, 1.286 - 6.241, P = 0.01) and doses of T cells (HR 3.059, CI, 1.292 - 7.246, P = 0.011) were independent risk factors for the acute graft versus host disease (aGVHD). In addition, compared to those without KIR ligand mismatch, patients with KIR ligand mismatch had the more adverse effect of 'high' dose T cells (> 1.48 x 10(5)/kg) on aGVHD (100% vs 63.3%, P = 0.036), and had more incidence of aGVHD with HLA-C mismatch (80.0% vs 57.4%, P = 0.056). Since multivariate analysis demonstrated that high risk leukemia was the only predictor for transplant related mortality (TRM), relapse and overall survival (OS), the effect of KIR ligand mismatch on prognosis in standard and high risk patients was further analyzed. The differences in TRM (50.0% vs 7.6%, P = 0.005) and OS (50.0% vs 88.4%, P = 0.014) between patients with and without KIR ligand mismatch were most striking for standard risk patients.

CONCLUSIONKIR ligand mismatch is a poor prognosis factor for patients underwent HLA mismatched HSCT, and is a useful parameter for donor selection.

Adolescent ; Adult ; Child ; Child, Preschool ; Female ; Graft vs Host Disease ; prevention & control ; HLA Antigens ; immunology ; Hematopoietic Stem Cell Transplantation ; Humans ; Male ; Middle Aged ; Multivariate Analysis ; Prognosis ; Receptors, KIR ; immunology ; Retrospective Studies ; Young Adult

OBJECTIVETo explore the potential of iodized linoleic acid (ILA) and its 5-fluoro-deoxyuridine ester (IFU) to inhibit hepatocellular carcinoma (HCC) cells in vitro and tumors in vivo.

METHODSILA and its constituent component IFU were chemically synthesized, purified, and confirmed by 1H-NMR. The HCC cell lines, QGY-7703 (5-fluorouracil (5-FU) treatment sensitive) and SMMC-7721 (5-FU resistant), were treated with ILA, IFU, 5-FU, or traditional lipiodol for 72 hours. Survival rates of the treated cells were assessed by the methyl thiazolyl tetrazolium method, and used to calculate the IC50 and IC90. In addition, thirty nude mice were subcutaneously inoculated with SMMC-7721 cells and randomly divided two weeks later into four treatment groups (n = 6 each) for intra-tumoral injection of ILA, IFU, 5-FU, lipiodol or DMSO (controls). The rate of tumor inhibition (RTI) was calculated for each group at week 4 after treatment.

RESULTSFor the cultured SMMC-7721 cells, the inhibitory concentrations for ILA, IFU, and 5-FU were: IC50: 134.38 mumol/L, 17.55 mumol/L, and 7.38 mumol/L; IC90: 192.88 mumol/L, 97.63 mumol/L, and more than 200 mumol/L. For the cultured QGY-7703 cells, the inhibitory concentrations for ILA, IFU, and 5-FU were: IC50: 109.55 mumol/L, 44.79 mumol/L, and 98.06 mumol/L; IC90: all, more than 200 mumol/L. In both cell types, the IC50 of lipiodol was more than 400 mumol/L. Compared with the RTI of the control mice (100%), the RTI of ILA-treated mice was 31.9% (t = 2.37, P less than 0.05), of IFU-treated mice was 56.9% (t = 4.91, P less than 0.01), and of 5-FU-treated mice was 31.0% (t = 2.59, P less than 0.05). The RTI of IFU was significantly stronger than that of either ILA or 5-FU (P less than 0.05). The lipiodol treatment showed no inhibition effect on tumors (P more than 0.05).

CONCLUSIONILA and IFU can effectively inhibit the growth of HCC cells in vitro and tumors in vivo. Furthermore, IFU outperforms ILA in inhibiting HCC growth.

Animals ; Carcinoma, Hepatocellular ; pathology ; Cell Line, Tumor ; Fluorouracil ; pharmacology ; Humans ; Inhibitory Concentration 50 ; Linoleic Acid ; pharmacology ; Liver Neoplasms ; pathology ; Male ; Mice ; Mice, Inbred BALB C ; Mice, Nude ; Xenograft Model Antitumor Assays