Objective To explore the interaction between serum melatonin and the status of disease and probe the effect factor of serum melatonin change in asthmatic children.Methods Serum melatonin was measured in asthmatic children with 15 cases of mild persistent asthma,15 cases of moderate persistent asthma,15 cases of severe persistent asthma,15 cases of stable asthma and 15 cases of normal subjects by enzyme-linked immunosorbent assay(ELISA).Results The levels of serum melatonin in the 5 groups of mild persistent asthma,moderate presistent asthma,Severe Persistent asthma,Stable asthma,control subject were(22.76?5.16)ng/L,(16.79?3.35)ng/L,(11.54?1.45)ng/L,(22.06?3.36)ng/L,(28.72?4.32)ng/L,respectively.There were significant differences between any of them(Pa

OBJECTIVETo observe the proliferation changes of the side population of gastric cancer cell line SGC-7901 cells (SP), the non-side population (NSP) cells, and unsorted cells (Total) after intervened by Sijunzi Decoction (SD) containing serum.

METHODSSixteen pure bred New Zealand rabbits were equally divided into the normal control group, the low dose SD group (at the daily dose of 7 mL/kg), the middle dose SD group (at the daily dose of 14 mL/kg), and the high dose SD group (at the daily dose of 28 mL/kg) according to the random digit table. Rabbits' serum was extracted after equal volume of corresponding medication was given by gastrogavage twice daily for 2 consecutive weeks. The drug serum was identified using high performance liquid chromatography. SP cells of SGC-7901 were detected using flow cytometry, SP and NSP cells were screened. The proliferation curve of SP, NSP, and Total cells were detected with CCK-8 assay. Changes of their proliferation were also observed.

RESULTSGinsenoside Rg1, an effective ingredient in SD was detected in prepared drug serum. The proliferation of SGC-7901 SP cells was significantly higher than that of NSP cells and Total cells (P < 0.05). Drug serum on gastric cancer cell line SGC-7901 SP, NSP, and Total cells could inhibit their proliferation, but its inhibition on SP cells' proliferation was significantly lower than on NSP and Total cells (P < 0.05).

CONCLUSIONSSD could significantly inhibit the proliferation of gastric cancer cell line SGC-7901 SP, NSP, and Total cells. But there exist obvious difference in the inhibition among the three groups.

Animals ; Cell Line, Tumor ; Cell Proliferation ; drug effects ; Drugs, Chinese Herbal ; pharmacology ; Humans ; Rabbits ; Side-Population Cells ; drug effects ; pathology ; Stomach Neoplasms ; pathology

OBJECTIVETo investigate the chemical constituents of Ilex pernyi.

METHODThe chemical constituents were isolated by various column chromatographic methods. The structures were identified by spectral data.

RESULTEight triterpenoid compounds were isolated and identified as ursolic acid (1), lupeol (2), alpha-amyrin (3), uvaol (4), 3beta-hydroxyurs-11-ene-13beta-olide (5), pomolic acid (6), lup-20 (29)-ene-3beta, 24-diol (7), 3beta, 23-dihydroxy-urs-12-en-28-oic acid (8).

CONCLUSIONThe eight compounds were obtained from this plant for the first time.

Ilex ; chemistry ; Oleanolic Acid ; analogs & derivatives ; chemistry ; isolation & purification ; Plant Leaves ; chemistry ; Plants, Medicinal ; chemistry ; Triterpenes ; chemistry ; isolation & purification

A new compound and five known compounds were isolated from the ethanolic extract of the leaves of Ilex pernyi Franch. Their structures were established on the basis of spectral analysis and identified as trans-isoeugenyl-alpha-L-arabinopynosyl (1 --> 6) -beta-D-glucopyranoside (1) , kaempferol-3-O-sambubioside (2), quercetin-3-O-sambubioside (3), isoquercitrin (4), (+) -syringaresinol-O-beta-D-glucopyranoside (5), amarantholidoside IV (6). Among them, compound 1 is a new phenolic glycoside, named as ilexperphenoside A, and compounds 2-6 were isolated from this plant for the first time.
Glucosides ; chemistry ; isolation & purification ; Glycosides ; chemistry ; isolation & purification ; Ilex ; chemistry ; Molecular Structure ; Plant Leaves ; chemistry ; Plants, Medicinal ; chemistry ; Quercetin ; analogs & derivatives ; chemistry ; isolation & purification

To explore the mechanisms of suppression growth and induction apoptosis of curcumin on human multiple myeloma cell line RPMI8226, the suppressive effect of curcumin on RPMI8226 was examined by MTT assay; the induction apoptosis and cell cycle arrest of curcumin on RPMI8226 were determined by flow cytometry (FCM); the changes of survivin, Bcl-2, Bax mRNA levels were detected by RT-PCR. The results showed that curcumin obviously suppressed the proliferation of RPMI8226 in both time- and dose-dependent manners, and the IC(50) were 12.15 micromol/L, 4.9 micromol/L for 24 and 48 hours respectively. FCM indicated that the apoptosis ratio rose from 10.6% of untreated cells up to 36.9% of treated cells (p < 0.05), and curcumin arrested cell cycle of RPMI8226 at G(2)/M phase. RT-PCR showed that RPMI8226 cells expressed survivin, Bcl-2 strongly and Bax slightly; while RPMI8226 cells were treated with curcumin 10 micromol/L for 24 hours, the expressions of survivin, Bcl-2 mRNA were apparently down-regulated, and the expression of Bax mRNA was markedly up-regulated. It is concluded that curcumin can suppress the proliferation of human multiple myeloma cell line RPMI8226, and induce their apoptosis. The mechanism of antitumous effect of curcumin may be related to down-regulation of survivin, Bcl-2 mRNA and up-regulation of Bax mRNA.
Antineoplastic Agents ; pharmacology ; Apoptosis ; drug effects ; Cell Line, Tumor ; Cell Proliferation ; drug effects ; Curcumin ; pharmacology ; Humans ; Inhibitor of Apoptosis Proteins ; Microtubule-Associated Proteins ; metabolism ; Multiple Myeloma ; metabolism ; pathology ; Proto-Oncogene Proteins c-bcl-2 ; metabolism ; RNA, Messenger ; metabolism

BACKGROUNDThe expression of the co-stimulatory molecule CD28 and death receptor CD95 on T cells, which change with age, are considered as important immunological parameters of immunosenescence. It is well established that CD28 and CD95 are associated with tumorgenesis and tumor progression, but the relationship between the age-related changes of these two immunological markers and cancer in the elderly is largely unknown.

METHODSThe levels of CD28 and CD95 mRNA in peripheral blood mononuclear cells (PBMCs) from sixty-three elderly patients (aged > or = 60 years) with primary non-small cell lung cancer (NSCLC) were analyzed by real-time fluorescence-based quantitative polymerase chain reaction (FQ-PCR). In addition, twenty young patients (aged < 60 years) with NSCLC, thirty elderly healthy donors and thirty young healthy donors were enrolled as controls.

RESULTSCD28 mRNA levels were significantly lower and CD95 mRNA levels were significantly higher in elderly patients with NSCLC than in the other groups. Similar results were found in elderly healthy donors comparing with young healthy donors. By Logistic regression analysis an increased risk of NSCLC was markedly associated with aging, down-regulation of CD28 mRNA and up-regulation of CD95 mRNA, and CD28 mRNA had an obvious negative correlation with the CD95 mRNA. In addition, the mRNA levels of CD28 and CD95 in the peripheral blood of the elderly patients was closely associated with the tumor node metastasis (TNM) stages, grade of cell differentiation and lymph node metastasis status, but not related to pathological types.

CONCLUSIONSThe results suggest a close relationship between T cell senescence and NSCLC tumour progress in the elderly, and that up-regulation of CD28 mRNA or down-regulation of CD95 mRNA in peripheral blood T cells may play an important role in inhibiting oncogenesis and development of primary NSCLC in the elderly.

Aged ; CD28 Antigens ; genetics ; Carcinoma, Non-Small-Cell Lung ; genetics ; Humans ; Leukocytes, Mononuclear ; metabolism ; Logistic Models ; Lung Neoplasms ; genetics ; Polymerase Chain Reaction ; fas Receptor ; genetics

BACKGROUNDThe pathophysiology of type 2 diabetes is progressive pancreatic beta cell failure with consequential reduced insulin secretion. Glucotoxicity results in the reduction of beta cell mass in type 2 diabetes by inducing apoptosis. Autophagy is essential for the maintenance of normal islet architecture and plays a crucial role in maintaining the intracellular insulin content by accelerating the insulin degradation rate in beta cells. Recently more attention has been paid to the effect of autophagy in type 2 diabetes. The regulatory pathway of autophagy in controlling pancreatic beta cells is still not clear. The aim of our study was to evaluate whether liraglutide can inhibit apoptosis and modulate autophagy in vitro in insulinoma cells (INS-1 cells).

METHODSINS-1 cells were incubated for 24 hours in the presence or absence of high levels of glucose, liraglutide (a long-acting human glucagon-like peptide-1 analogue), or 3-methyadenine (3-MA). Cell viability was measured using the Cell Counting Kit-8 (CCK8) viability assay. Autophagy of INS-1 cells was tested by monodansylcadaverine (MDC) staining, an autophagy fluorescent compound used for the labeling of autophagic vacuoles, and by Western blotting of microtubule-associated protein I light chain 3 (LC3), a biochemical markers of autophagic initiation.

RESULTSThe viability of INS-1 cells was reduced after treatment with high levels of glucose. The viability of INS-1 cells was reduced and apoptosis was increased when autophagy was inhibited. The viability of INS-1 cells was significantly increased by adding liraglutide to supplement high glucose level medium compared with the cells treated with high glucose levels alone.

CONCLUSIONSApoptosis and autophagy were increased in rat INS-1 cells when treated with high level of glucose, and the viability of INS-1 cells was significantly reduced by inhibiting autophagy. Liraglutide protected INS-1 cells from high glucose level-induced apoptosis that is accompanied by a significant increase of autophagy, suggesting that liraglutide plays a role in beta cell apoptosis by targeting autophagy. Thus, autophagy may be a new target for the prevention or treatment of diabetes.

Animals ; Apoptosis ; drug effects ; Autophagy ; drug effects ; Cell Line, Tumor ; Cell Survival ; drug effects ; Glucagon-Like Peptide 1 ; analogs & derivatives ; pharmacology ; Glucose ; pharmacology ; Insulinoma ; pathology ; Liraglutide ; Rats

OBJECTIVETo find out the differentially expressed genes in the hippocampus of the rats with genetic epilepsy so as to lay a foundation for exploring the pathogenesis of epilepsy by means of cDNA array technology.

METHODSGene expression patterns in the hippocampus of the genetic epilepsy-prone P77PMC rats and normal Wistar rats were established using the alpha-32P-labeled cDNA probes hybridized with the Atlas Rat cDNA Expression Array, and then were analyzed by an image analysis instrument to get the differentially expressed genes.

RESULTSFifteen genes were found having differential expression patterns in hippocampus between the P77PMC rats and the Wistar rats, while there may be many other differentially expressed genes left undiscovered due to having no appropriate image analysis software. And among the fifteen genes, the expression levels of twelve genes in the P77PMC rats were higher than those in the Wistar rats, while the expression levels of the other three genes were lower. The results of reverse transcription-polymerase chain reaction(RT-PCR) have demonstrated the reliability of cDNA arrays method.

CONCLUSIONcDNA array is a powerful tool for identifying differential expression genes of epilepsy on large scales. There are several differentially expressed genes in hippocampus of the P77PMC rats and the Wistar rats. All these identified genes could play potentially important roles in the pathogenesis of epilepsy.

Animals ; Calmodulin ; biosynthesis ; genetics ; DNA, Complementary ; genetics ; metabolism ; Epilepsy ; genetics ; Gene Expression Profiling ; Genetic Predisposition to Disease ; Hippocampus ; chemistry ; metabolism ; Oligonucleotide Array Sequence Analysis ; RNA, Messenger ; biosynthesis ; genetics ; Rats ; Rats, Wistar ; Reverse Transcriptase Polymerase Chain Reaction

BACKGROUNDAfter T-cell depleted allogeneic bone marrow transplantation, impaired immune reconstitution is a major cause of morbidity and mortality in the recipient. The purpose of this study was to observe the effects of the gene-engineered bone marrow stromal cell line QXMSC1-IL-2 + IL-3 on the reconstitution of T-cell immunity in allo-BMT mice.

METHODSThe bone marrow stromal cell line QXMSC1 was co-transfected with IL-2 and IL-3 genes using a Tet-on gene expression system. T lymphocyte subset counts per spleen were analyzed by flow cytometry. Lymphocyte proliferation response to ConA was examined to evaluate T-cell function. CDR3 spectratyping techniques were performed to evaluate TCR repertoire diversity at various time points post-transplantation.

RESULTSGene engineered bone marrow stromal cell line QXMSC1-IL-2 + IL-3 could express IL-2 and IL-3 [1,300 ng.day(-1).10(-6) cells and 1100 ng.day(-1).10(-6) cells, respectively] under the control of doxycycline. QXMSC1-IL-2 + IL-3 in combination with allogeneic bone marrow could significantly increase the counts of CD(4)(+) and CD(8)(+) T cell, 1.72 and 1.27-fold respectively at week 3 compared with TCD-BMT group (P < 0.01); make CD(4)(+)/CD(8)(+) ratio return to normal level at week 4; enhance splenocytes mitotic response to ConA (P < 0.01), and accelerate restoration of TCR repertoire diversity in the lethally irradiated mice (P < 0.05).

CONCLUSIONThe gene transduced stromal cell line QXMSC1-IL-2 + IL-3 is able to accelerate T-cell immunity in allo-BMT mice.

Animals ; Bone Marrow Cells ; metabolism ; Bone Marrow Transplantation ; immunology ; Cell Line ; Complementarity Determining Regions ; Doxycycline ; pharmacology ; Female ; Interleukin-2 ; genetics ; Interleukin-3 ; genetics ; Mice ; Mice, Inbred BALB C ; Mice, Inbred C57BL ; Stromal Cells ; metabolism ; T-Lymphocytes ; immunology ; Transfection ; Transplantation, Homologous

OBJECTIVETo investigate the cough-relieving, analgesic and antibiotic effects of durian shell extract (DSE) in relieving cough and its analgesic and antibiotic effects.

METHODSThe effect of DSE in relieving cough was assessed in mice challenged with ammonia and SO(2) to induce coughing. The analgesic and antibiotic effects of DSE in mice were evaluated by hot plate test and twisting reaction induced by acetic acid, and by minimal inhibitory concentration (MIC) and disc-agar diffusion tests, respectively.

RESULTSCompared with the control group, the mice treated with 300 and 900 mg/kg DSE showed significantly prolonged latency with decreased number of coughing induced by ammonia and SO(2), and the effect was dose-dependent. DSE markedly prolonged the latency and decreased the twisting number of the mice induced by acetic acid without affecting the pain threshold in hot plate test. DSE produced no significant inhibitory effects against Staphylococcus aureus, Staphylococcus epidermidis, or E. coli, and showed a week inhibition against Bacillus aeruginosus.

CONCLUSIONDSE shows obvious effect in relieving cough and produces better analgesic effect against chemical factor-induced pain than against physical agent-induced pain sensation. DSE has a moderate inhibitory effect against Bacillus aeruginosus.

Analgesics ; pharmacology ; Animals ; Anti-Bacterial Agents ; pharmacology ; Antitussive Agents ; pharmacology ; Bombacaceae ; chemistry ; Male ; Mice ; Plant Extracts ; pharmacology ; Random Allocation