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Arrhythmia is an external manifestation of cardiac electrophysiological disorder. It exists in healthy people and patients with various heart diseases, which is often associated with other cardiovascular diseases. The contraction and diastole of myocardium are inseparable from the movement of ions. There are many ion channels in the membrane and organelle membrane of myocardium. The dynamic balance of myocardial ions is vital in maintaining myocardial electrical homeostasis. Potassium ion channels that have a complex variety and a wide distribution are involved in the whole process of resting potential and action potential of cardiomyocytes. Potassium ion channels play a vital role in maintaining normal electrophysiological activity of myocardium and is one of the pathogenesis of arrhythmia. Traditional Chinese medicine(TCM)has unique advantages in treating arrhythmia for its complex active components and diverse targets. A large number of TCM preparations have definite effect on treating arrhythmia-related diseases, whose antiarrhythmic mechanism may be related to the effect on potassium channel. This article mainly reviewed the relevant studies on the active components in TCM acting on different potassium channels to provide references for clinical drug use and development.
Subject(s)
Humans , Potassium Channels , Medicine, Chinese Traditional , Anti-Arrhythmia Agents/therapeutic use , Arrhythmias, Cardiac/drug therapy , Heart Diseases/drug therapy , IonsABSTRACT
The chigger mite Leptotrombidium sialkotense is one of the 6 main vectors of scrub typhus in China. Before present study, L. sialkotense was found in some parts of Hunan province, China with a narrow geographical distribution. During field investigation 2016-2017, we found L. sialkotense in Jingha, southern Yunnan, China. Of 15 small mammal host species, L. sialkotense were collected from 6 species of the hosts. Rattus brunneusculus was a dominant host of L. sialkotense, from which 98.3% of the mites were collected. The chigger mite showed a relatively high infestation prevalence (PM=11.7%) and mean abundance (MA=0.5) in comparison with the rest 5 host species. These results reveal a certain host specificity of L. sialkotense to a rat R. brunneusculus. The mite L. sialkotense showed an aggregated distribution on the host (P<0.05). A positive correlation observed between L. sialkotense and the body length of hosts. There was a positive interspecific association between L. sialkotense and 2 other dominant vectors, L. deliense and L. scutellare.
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Objective::To explore the possible mechanisms of Erzhiwan in the treatment of hepatocellular carcinoma (HCC) based on the network pharmacology. Method::The candidate active components and targets of Ligustri Lucidi Fructus and Ecliptae Herba were obtained through retrieval of the traditional Chinese medicine (TCM) systems pharmacology database (TCMSP) and literatures. Through Uniprot database and the human genome database (GeneCards), the overlapping genes of Erzhiwan and hepatocellular carcinoma were collected. The " candidate active components-targets" network of Ligustri Lucidi Fructus and Ecliptae Herba was built with Cytoscape 3.6.0 software. Drug target proteins and disease targets were mapped, and Venn map was drawn by Omicshare database. Major targets interaction network was formed by using String database and " Generate style from statistics" tool in Cytoscape 3.6.0 software. Molecular docking with active components was carried out by Systems Dock Web Site. The Gene Ontology (GO) classification enrichment analysis and the Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analysis for the targets were carried out in DAVID database. Result::Totally 21 active components, including beta-sitosterol, quercetin, luteolin, demethylwedelolactone, kaempferol, and 151 targets, including tumor necrosis factor (TNF), vascular endothelial growth factor (VEGF), N-terminal kinase (JUN), proto-oncogene (c-MYC), matrix metalloproteinase-9 (MMP-9) of Erzhiwan were collected. Erzhiwan exerts its effects on HCC mainly by acting on signal pathways, including Hepatitis B, TNF, Phosphatidylinositol-3-kinase (PI3K/Akt), tumor suppressor gene p53 and Toll-like receptor. Conclusion::Based on the methodology of network pharmacology, this study preliminarily predicted the major targets and pathways of Erzhiwan in the treatment of HCC, providing a direction for further studies.
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<p><b>OBJECTIVE</b>To observe the change of lipid metabolism and vascular endothelium as well as morphology of heart tissue in rats who were long-time exposed to moxa smoke with different concentrations in order to provide reference for safety assessment of moxa smoke on cardiovascular system.</p><p><b>METHODS</b>One hundred and sixty-eighty Wistar rats were randomly divided into a control group, a low-concentration group, a median-concentration group and a high-concentration group, 42 rats in each one. The rats were exposed to moxa smoke with concentration of 0%, 10%, 40% and 70%, respectively, for 20 min per day. After continuous intervention for six months, enzyme-linked immunosorbent assay (ELISA) was applied to measure the level of low density lipoprotein-receptor (LDL-r) and intercellular adhesion molecule-1 (ICAM-1) in blood serum in each group; the slices of heart tissue were stained with hematoxylin-eosin staining method to observe morphology change of heart tissue.</p><p><b>RESULTS</b>(1) After the intervention of moxa smoke, the levels of LDL-r and ICAM-1 in the low-concentration group were not statistically different from those in the control group (both P > 0.05); the level of LDL-r in the median-concentration group was significantly increased, which was statistically different from that in the control group [(3.87 +/- 0.27) mg/mL vs (2.12 +/- 0.13) mg/mL, P < 0.01], however, the content of ICAM-1 was not obviously changed; although the level of LDL-r in the high-concentration group was presented with an escalating trend, it was not statistically different from that in the control group (P > 0.05) while the level of ICAM-1 was obviously increased (P < 0.01). (2) Under the light microscope, the abnormalities of cardiac muscle fibers and myocardial cell in each group were not been observed.</p><p><b>CONCLUSION</b>The long-time intervention of low-concentration moxa smoke has no significant effects on lipid metabolism and vascular endothelium of rats, indicating that clinical application of low-concentration moxa smoke is relatively safe. The long-time intervention of moderate-concentration moxa smoke could significantly increase the clearance rate of cholesterol, implying the beneficial regulation of moxa smoke on lipid metabolism. The high-concentration moxa smoke could induce certain damage to vascular endothelium but its mechanism is in need of further research. The pathologic change of heart tissue could not be induced by moxa smoke with any concentration.</p>
Subject(s)
Animals , Male , Rats , Heart , Intercellular Adhesion Molecule-1 , Metabolism , Lipid Metabolism , Moxibustion , Myocardium , Pathology , Rats, Wistar , Receptors, LDL , Metabolism , SmokeABSTRACT
<p><b>OBJECTIVE</b>To investigate the cellular immune regulation of the long-term intervention of moxa smoke.</p><p><b>METHODS</b>Thirty-two Wistar rats were randomly divided into a blank group, a low concentration group, a medium concentration group and a high concentration group, 8 cases in each group. In addition to the blank group, rats in the other groups were exposed to the corresponding concentration moxa smoke for 20 min every day, the T lymphocyte subsets and proportion of the CD4+ CD25+ Treg in CD4+ T cells in peripheral blood were tested by flow cytometry after 6 months.</p><p><b>RESULTS</b>Compared with the blank group, the proportions of CD3+ CD4+, CD3+ CD8+ T cells and CD3+ CD4/CD3+ CD8+ in the other 3 moxa smoke groups were not significantly different (P > 0.05), while the proportions of the CD4+ CD25+ Treg in CD4+ T cells were significantly lower (P < 0.05), but no statistically significant differences among those 3 moxa smoke intervention groups (P > 0.05).</p><p><b>CONCLUSION</b>Long-term moxa smoke intervention has no significant effect on the proportions of CD3+ CD4+, CD3+ CD8+ T cells and CD3+ CD4+/CD3+ CD8+, but it can decrease the proportions of the CD4+ CD25+ Treg in CD4+ T cells in peripheral blood of rats. The way produced by pretreatment with moxa smoke may play immunomodulatory effect.</p>
Subject(s)
Animals , Male , Rats , Lymphocyte Count , Moxibustion , Rats, Wistar , Smoke , T-Lymphocyte Subsets , Allergy and Immunology , T-Lymphocytes, Regulatory , Allergy and Immunology , Time FactorsABSTRACT
<p><b>OBJECTIVE</b>To explore the toxic effects of lead acetate on the apoptosis and ultrastructure of human renal tubular epithelial cells (HK-2).</p><p><b>METHODS</b>After HK-2 cells were exposed to 5, 10 and 20 µmol/L lead acetate for 24 h, the morphological changes of HK-2 cells were observed by Hochest 33342-PI staining, and the ultrastructure changes of HK-2 cells were examined under a electron microscope, LDH activity and MDA content in supernatant of HK-2 cellular culture were detected by spectrophotometer, DNA damage of HK-2 was determined by DNA ladder and the apoptotic rates of HK-2 cells were measured by flow cytometry.</p><p><b>RESULTS</b>The morphological changes of apoptotic HK-2 cells in exposure group were observed by Hochest 33342-PI staining. The cytoplasm vacuoles, karyopycnosis, nuclear membrane vague and apoptotic bodies in HK-2 cells of exposure group were found under electron microscopy. LDH activity and MDA contents in exposure group increased significantly, as compared to control group (P < 0.01). The results of DNA Ladder showed that DNA damage of HK-2 cells in exposure group appeared. The apoptotic rates of HK-2 cells exposed to 5, 10, 20 µmol/L lead acetate were 14.16% ± 2.94%, 19.45% ± 2.73%, 25.01% ± 3.97%, respectively, which were significantly higher than that (5.81% ± 2.18%) in control group (P < 0.05).</p><p><b>CONCLUSION</b>Lead acetate could remarkably induce the apoptosis of HK-2 cells and affect the kidney.</p>
Subject(s)
Humans , Apoptosis , Cell Line , Epithelial Cells , Cell Biology , Kidney Tubules, Proximal , Cell Biology , Organometallic Compounds , ToxicityABSTRACT
<p><b>OBJECTIVE</b>The purpose of this study was to construct a pathway-based network using differentially expressed genes in prostate cancer (PCa) screened by cDNA microarray chips in domestic research to visualize the relations among the genes obtained from the microarray data, and identify the genes with significant influence on this network by statistical analysis. It also aimed to search for the genes that play key roles in the tumorigenesis of PCa, and probe into the molecular mechanism of PCa pathogenesis in Chinese men.</p><p><b>METHODS</b>The relevant domestic literature of recent years were reviewed to sum up differentially expressed genes in PCa according to the screened microarray data. The OMIM database was used to analyze the relations among these genes and build a network of biological pathway. Furthermore, a statistical method, namely node contraction, was employed to compare the importance of the key genes.</p><p><b>RESULTS</b>According to the gene expression profiling data, there were 113 differentially expressed genes, 51 up-regulated and 62 down-regulated. A pathway-based network including 68 inter-related genes was constructed using the OMIM database. The importance of every key node was calculated using the method of node contraction, and 12 key genes were identified, incuding c-MYC, VEGF, HSPCA, TGFbeta1, RANTES, EGR1, etc, which probably played important roles in the pathogenesis and progression of prostate cancer.</p><p><b>CONCLUSION</b>We applied bioinformatics to the analysis of the gene expression profiling data in China, constructed a network of the differentially expressed genes using the OMIM database and method of node contraction, appraised the importance of the key genes, and established a method for the overall analysis of the gene chip data, which have paved a new ground for further researches on the pathogenesis of prostate cancer in Chinese men.</p>
Subject(s)
Humans , Male , Asian People , Genetics , Computational Biology , Methods , Databases, Genetic , Gene Expression Profiling , Gene Expression Regulation, Neoplastic , Oligonucleotide Array Sequence Analysis , Prostatic Neoplasms , Genetics , MetabolismABSTRACT
<p><b>BACKGROUND</b>Thrombin is a multifunctional serine protease that plays a crucial role in hemostasis following tissue injury. In addition to its procoagulation effect, thrombin is also a potent mesenchymal cell mitogen, therefore it plays important roles in the local proliferation of mesenchymal cells in the tissue repair process. Reactive oxygen species (ROS) can induce some human cells to proliferate at lower rates while at higher concentrations they promote cells to undergo apoptosis or necrosis. Accumulative evidence suggests that thrombin can induce some cells to produce ROS. Based on these observations, we provide a hypothesis that thrombin can stimulate human lung fibroblasts to produce ROS, which play an important role in human lung fibroblast proliferation.</p><p><b>METHODS</b>ROS were detected in fibroblasts at 30 minutes and 60 minutes following thrombin (20 U/ml) exposure using flow cytometry. The ratio of reduced glutathione/oxidized glutathione (GSH/GSSG) was assayed in lung fibroblasts using a commercial kit following treatment with thrombin at different concentrations. NADPH oxidase and the extracellular regulated kinase1/2 (ERK1/2) signaling pathway were detected by Western blotting after thrombin stimulation to lung fibroblasts.</p><p><b>RESULTS</b>Thrombin, at 20 U/ml, stimulated human lung fibroblasts (HLF) to generate ROS in a time dependent manner. The ratio of GSH/GSSG in fibroblasts treated with thrombin showed a significant decrease. NADPH oxidase was activated and the ERK1/2 signal pathway was involved in the proliferation process of fibroblasts treated with thrombin.</p><p><b>CONCLUSION</b>The activation of NADPH oxidase by thrombin leads to the production of ROS, which promotes fibroblasts proliferation via activation of the ERK1/2 signaling pathway.</p>
Subject(s)
Humans , Cell Proliferation , Cells, Cultured , Extracellular Signal-Regulated MAP Kinases , Physiology , Fibroblasts , Physiology , Flow Cytometry , Glutathione , Metabolism , Lung , Cell Biology , NADPH Oxidases , Physiology , Reactive Oxygen Species , Metabolism , Signal Transduction , Physiology , Thrombin , PharmacologyABSTRACT
<p><b>OBJECTIVE</b>To establish a novel suspension microarray technology for the detection of three kinds of veterinary drug residues: chloramphenicol, clenbuterol and 17-beta-estradiol (CAP, CL and E2).</p><p><b>METHODS</b>The three conjugates that veterinary drug coupled with bovine serum albumin (BSA) were synthesized and identified by ultraviolet (UV) spectrophotometry and mass spectrum. The veterinary drug conjugates were immobilized on the polystyrene fluorescent microspheres/beads. There were competitive reactions between the veterinary drugs in the aqueous phase and that on the beads for combination with their specific biotinylated monoclonal antibodies. The optimum amount of the veterinary drug conjugates and the antibodies were optimized and selected. The detective standard curves were plotted. The specificity and the unknown samples were also determined by grouping according to different concentrations of the interferes and the samples. Meantime, the different microstructures of the surfaces of the beads were also observed by scanning electron microscope.</p><p><b>RESULTS</b>Couplings were completed between small molecular veterinary drugs and BSA. The amounts of the three conjugates and the antibodies were optimized. The detective standard curves of the suspension array and their corresponding coefficients of determination (R2) were good (R2 > 0.99). The detection ranges of the three veterinary drugs were (40.00 - 6.25) x 10(5) ng/L, (50.00-7.81) x 10(5) ng/L and 1.00 x 10(3) - 7.29 x 10(5) ng/L respectively. Simultaneously, the specific detection of the suspension microarray was excellent and did not indicate significant cross-reactions. Errors between the found and the real are in the range of 8.09% - 17.03%. It can be considered that the relative standard deviations were relatively small. Successful couplings were also directly confirmed by the observation for microstructures of the surfaces of the beads by scanning of electron microscope and laid good foundation for the following responses.</p><p><b>CONCLUSION</b>The high-throughput suspension microarray should provide a novel method for multi-analysis of the veterinary drugs and have a wide applicative prospects with simple operation, sensitive, rapid and low cost.</p>
Subject(s)
Chloramphenicol , Clenbuterol , Drug Residues , Estradiol , Microarray Analysis , Methods , Veterinary DrugsABSTRACT
<p><b>OBJECTIVE</b>To further explore the effect of annexin I on the tumor growth of human pancreatic cancer in nude mice.</p><p><b>METHODS</b>To knock down the expression of annexin I in pancreatic carcinoma cells by RNAi. A nude mouse model of human pancreatic cancer was established by subcutaneous inoculation of human pancreatic cancer cell line Suit-II cells. The effect of annexin I on tumor growth was assessed by tumor growth curve and tumor weight records, and Westen blot and flow cytometry were used to examine the expression of annexin I after annexin I-knocking down.</p><p><b>RESULTS</b>The results of Western blot revealed that the expression of annexin I was significantly decreased in Suit-II cells transfected with pSilencer-annexin I-siRNA1, and almost completely inhibited in the cells transfected with pSilencer-annexin I-siRNA2 and pSilencer-annexin I-siRNA3. The growth of tumors transfected with annexin I-siRNA2 and annexin I-siRNA3 was inhibited by 76.6% and 68.4%, respectively, in comparison with that of tumor from the parent Suit-II cells. At 44 days after tumor cell inoculation, the tumor weight was 0.8987 g (transfected with annexin I-siRNA2) and 0.8992 g (transfected with annexin I-siRNA3), significantly lower (P < 0.001) than that of tumor from parent Suit-II cells (2.5866 g) and transfected with annexin I-siRNAN (2.4070 g).</p><p><b>CONCLUSION</b>annexin I promotes the growth and proliferation of pancreatic carcinoma cells in vivo and increases the ability of tumor formation in nude mice. The results of this study support that annexin I may become a potential target in gene therapy for this disease.</p>
Subject(s)
Animals , Female , Humans , Mice , Annexin A1 , Genetics , Metabolism , Cell Line, Tumor , Cell Proliferation , Down-Regulation , Gene Expression Regulation, Neoplastic , Genetic Vectors , Mice, Nude , Neoplasm Transplantation , Pancreatic Neoplasms , Genetics , Pathology , RNA Interference , RNA, Small Interfering , Genetics , Transfection , Tumor BurdenABSTRACT
<p><b>OBJECTIVE</b>To investigate the role of adhesion molecules alphavbeta3 and alphavbeta5 and their ligands Del-1 and L1 in the tumor-endothelial cell adhesion in vitro.</p><p><b>METHODS</b>The expression of alphavbeta3, alphavbeta5 and ICAM-1 in liver sinusoidal endothelial cells (LSEC) and liver cancer endothelial cells (T3A) cultured under normoxia or hypoxia were analyzed by RT-PCR and fluorescent activated cell sorter (FACS). The expression of Del-1 and L1 in six tumor cell lines under normoxia or hypoxia were analyzed by RT-PCR and Western blot, respectively. The adhesion of dye-labeled tumor cells and endothelial LSEC and T3A cells was measured by a fluorescence plate reader after their culture.</p><p><b>RESULTS</b>The expression of alphavbeta3 and alphavbeta5 were higher in T3A cells than that in LSEC cells, and were upregulated under hypoxia, while the expression of ICAM-1 was lower in T3A cells than that in LSEC cells, and was upregulated under hypoxia only in LSEC. The expression of Del-1 and L1 molecules were obviously different in various tumor cell lines and were differentially regulated under hypoxia. The adhesion of tumor cells with Del-1 or L1 expression was higher in T3A cells than that in LSEC cells, and was significantly increased under hypoxia condition. Furthermore, the adhesion of tumor cells to T3A could be inhibited by antibodies against alphavbeta3 and alphavbeta5, or SiRNAs for beta3 and beta5.</p><p><b>CONCLUSION</b>alphavbeta3 and alphavbeta5 and their ligands Del-1 and L1 may play an important role in tumor cell migration.</p>
Subject(s)
Humans , Antibodies , Allergy and Immunology , Cell Adhesion , Cell Hypoxia , Cell Line, Tumor , Endothelial Cells , Cell Biology , Metabolism , Integrin alphaVbeta3 , Genetics , Allergy and Immunology , Metabolism , Intercellular Adhesion Molecule-1 , Allergy and Immunology , Metabolism , Ligands , Neoplasms , Metabolism , Pathology , RNA Interference , RNA, Messenger , Metabolism , RNA, Small Interfering , Pharmacology , Receptors, Vitronectin , Genetics , Allergy and Immunology , MetabolismABSTRACT
<p><b>AIM</b>To assay the transcriptional activation effect of TR3 and it's deletion mutation in yeast two hybrid system.</p><p><b>METHODS</b>The total length of TR3 and TR3/delta1-690 gene was amplified by PCR method and cloned into pGBKT7 vector. Bait vector of pGBKT7-TR3 and pGBKT7-TR3/delta1-690 was transformed into AH109 competence yeast. Then self activation of the recombination vector was tested by assay the activity of beta-galactosidae.</p><p><b>RESULTS</b>The pGBKT7-TR3 and pGBKT7-TR3/AM 690 vector was successfully constructed. The filter paper containing beta-galactosidae didn't changed to blue showed that the reporter gene wasn't activationed.</p><p><b>CONCLUSION</b>TR3 and TR3/delta1-690 hadn't the activity of transcriptional activation.</p>
Subject(s)
Nuclear Receptor Subfamily 4, Group A, Member 1 , Genetics , Physiology , Sequence Deletion , Transcriptional Activation , Genetics , Two-Hybrid System TechniquesABSTRACT
<p><b>OBJECTIVE</b>To analyze the phenotypic and functional characteristics of endothelial (T3A) cells derived from human hepatocellular cell carcinoma.</p><p><b>METHODS</b>Endothelial cells were isolated from human hepatocellular carcinoma specimens. The identification of T3A cells was performed by checking von Willebrand Factor (vWF), CD31, CD34 and Dil-Ac-LDL uptake. The cell surface fenestrations, a specific morphological feature of tumor derived EC, were investigated by scanning and transmission electron microscopy. The phenotypic characteristics of T3A cells were analyzed by fluorescence-activated cell sorter (FACS) and were further conformed by real-time PCR at transcription level. Furthermore, tumor necrosis factor alpha (TNFalpha)-induced cytotoxicity was evaluated by 3-(4, 5-dimethythiazolyl) -2, -diphenyl-2H-tetrazolium-bromide (MTT) assay; Matrix metalloproteinase secretion was detected by zymography; Angiogenic ability in vitro was analyzed by culturing T3A cells in three-dimensional Matrigel plug. Coagulant and fibrinolytic activities were detected by enzyme-linked immunosorbent assay (ELISA).</p><p><b>RESULTS</b>The isolated T3A cells exhibited classic "spindle-shape" morphology and monolayer growth and contact inhibition properties. Immunofluorescent staining showed that T3A cells expressed vWF, CD31, CD34, and uptake of Dil-Ac-LDL at a high level. The cell surface fenestrations were observed on T3A cells by scanning and transmission electron microscopy. By FACS and real-time PCR, T3A cells were found to express alphav3, alphavbeta5 and TNF receptor p75 at high levels, and TNF receptor p55 and ICAM-1 at low levels, as compared with those in human liver sinusoidal endothelial cells (LSEC). In response to TNFalpha, LSEC exhibited a dose-dependent cytotoxicity, while T3A cells were resistant. Gelatin zymography showed that MMP-2 activity was higher in T3A cells than that in LSEC. In a three-dimensional plug of Matrigel, T3A cells exhibited stronger angiogenic ability as compared with LSEC. In addition, T3A cells released more tissue factor (TF), tissue-type plasminogen activator (t-PA), plasminogen activator inhibitor (PAI-1) and urine plasminogen activator (u-PA) than LSEC in response to TNFalpha.</p><p><b>CONCLUSION</b>Tumor-derived endothelial cells are phenotypically and functionally different from those derived from normal liver tissue.</p>
Subject(s)
Humans , Antigens, CD34 , Metabolism , Carcinoma, Hepatocellular , Genetics , Metabolism , Pathology , Cell Proliferation , Cell Shape , Cells, Cultured , Endothelial Cells , Metabolism , Pathology , Gene Expression , Integrin alphaVbeta3 , Metabolism , Integrins , Metabolism , Intercellular Adhesion Molecule-1 , Metabolism , Lipoproteins, LDL , Metabolism , Liver Neoplasms , Genetics , Metabolism , Pathology , Lung , Metabolism , Pathology , Matrix Metalloproteinase 2 , Metabolism , Microscopy, Electron, Scanning , Neovascularization, Pathologic , Metabolism , Pathology , Phenotype , Plasminogen Activator Inhibitor 1 , Metabolism , Platelet Endothelial Cell Adhesion Molecule-1 , Metabolism , Receptors, Tumor Necrosis Factor, Type I , Metabolism , Receptors, Vitronectin , Metabolism , Tissue Plasminogen Activator , Metabolism , Tumor Cells, Cultured , Tumor Necrosis Factor Decoy Receptors , Metabolism , Tumor Necrosis Factor-alpha , Pharmacology , von Willebrand Factor , MetabolismABSTRACT
<p><b>AIM</b>To approach the expression of prohibitin in oxidative stressed cardiomyocytes.</p><p><b>METHODS</b>The oxidative stress model was established by treating neonatal cardiomyocytes with H2O2. Injury of cardiomyocytes were evaluated by detecting the LDH activity and MTT cell survival rate.The expression level of prohibitin was examined via the Western-blotting. The ability of mitochondrial oxidative phosphorylation was determined by measuring ATP synthesis via H+ -ATPase. Mitochondrial membrane potential was detected by flow cytometry using Rhl23.</p><p><b>RESULTS</b>LDH activity increased significantly after exposure to H202, while the cell survival rate decreased by 34.51%-65.5%. The contents of mitochondrial prohibitin in stress group was much higher than that in control group. At the same time, the ability of ATP synthesis decreased by 60% and mitochondrial transmembrane potential decreased too.</p><p><b>CONCLUSION</b>Express of prohibitin in oxidative stress cardiomyocytes was compensated increase. Prohibitin translocated to mitochondria after oxidative stress. Oxidative stress led to mitochondrial dysfunction.</p>
Subject(s)
Animals , Rats , Apoptosis , Cells, Cultured , L-Lactate Dehydrogenase , Metabolism , Mitochondria, Heart , Metabolism , Myocytes, Cardiac , Metabolism , Pathology , Oxidative Stress , Rats, Wistar , Repressor Proteins , MetabolismABSTRACT
<p><b>AIM</b>To elucidate the mechanism of depression induced by chronic unpredictable mild stress (CUMS), the effects of CUMS on serotonin (5-HT), tryptophan, stress hormones and behaviour were investigated in rats.</p><p><b>METHODS</b>Depression was induced by for 8 weeks CUMS and confirmed by behavioral tests, the brain and plasma levels of monoamine neurotransmitters were analyzed by HPLC-ECD techniques, the content of plasma corticosterone was evaluated by I125 cortisol radioactivity immunoassay and the serum tryptophan content was measured by HTTACHI L-8800 amino acid analyzer.</p><p><b>RESULTS</b>(1) Rats exposed to a series of mild, unpredictable stressors for 8 weeks displayed the decreased body weight, reduced scores of open-field test and preference of sucrose solution (P < 0.05). (2) Plasma and brain 5-HT contents in rats after exposure to CUMS 8 weeks decreased significantly (P < 0.05). While serum tryptophan content increased at the same time (P < 0.05). (3) Plasma norepinephrine and epinephrine in rats were increased after CUMS 8 weeks, but there was no difference between control and CUMS group in plasma corticosterone.</p><p><b>CONCLUSION</b>The behavioral changes induced by CUMS for 8 weeks are similar to the features of human depression, which may be related to the disturbances of tryptophan metabolism induced by increased norepinephrine and epinephrine in CUMS rat.</p>
Subject(s)
Animals , Male , Rats , Depression , Metabolism , Epinephrine , Metabolism , Hippocampus , Metabolism , Neurosecretory Systems , Metabolism , Norepinephrine , Metabolism , Rats, Wistar , Serotonin , Metabolism , Stress, Psychological , MetabolismABSTRACT
@#Objective To observe the therapeutic effect of plum-blossom needle therapy and cupping therapy combined with traction on cervical spondylosis of vertebral artery type.Methods 60 patients with cervical spondylosis of vertebral artery type were randomly divided into the treatment group and control group with 30 cases in each group. The patients of the treatment group were treated with plum-blossom needle therapy and cupping therapy combined with traction, and those of the control group only with traction. The therapeutic effects of two groups were compared.Results The total effective rate of the treatment group was 83.3 %, that of the control group was 60.0%. There was a significant difference between two groups ( P<0.05).Conclusion The effect of plum-blossom needle therapy and cupping therapy combined with traction on cervical spondylosis of vertebral artery type is superior to traction therapy alone.
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Objective To explore epithelial ovarian cancer(EOC)antigens that are potentially useful for cancer early detection and therapy.Methods A high quality cDNA library derived from ascites tumor cells of EOC patients(3 cases of serous EOC,1 case of mucinous EOC,and 1 case of endometrial carcinoma of ovary)was constructed,and the method of combining serological analysis of recombinant cDNA expression libraries(SEREX)and suppression subtractive hybridization(SSH)was used for screening cDNA library.All of the positive clones were sequenced and bioinformatics analysis with BLAST software in GenBank was performed.Serological mini-arrays of recombinant tumor antigens(SMARTA)was used to investigate the prevalence of autoantibodies to these antigens in both 96 ovarian cancer patients and 96 cancer-free controls.Results Fifty-five positive clones encoding different antigenic genes of EOC recognized by IgG and(or)IgM were obtained.It showed that these 55 clones derived from 45 distinct genes and these genes could be grouped into 6 classes as following according to homology with known expressed sequence tag(EST):(1)known ovarian carcinoma related genes:BARD1,et al;(2)homologous genes with other tumors:TM4SF1,et al;(3)homologous genes with special tissues:ILF3,FXR1,et al;(4) homologous genes with special function:TIZ,C1 D,et al;(5)embryo originating genes:PKHD1,et al; (6)novel genes:OV-189,et al.SMARTA results showed that the positive ratio of five EOC antigens TM4SF1(28% vs 9%),CID(21% vs 6%),BARD1(23% vs 5%),FXR1(23% vs 8%),OV-189 (31% vs 13%)which reacting with their IgG autoantibodies,three antigens TIZ(26% vs 8%),FXR1 (28% vs 11%),and OV-189(18% vs 7%)which reacting with their IgM autoantibodies in patients was higher than in controls(P