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Objective:To analyze the adverse reactions of patients with multidrug-resistant pulmonary tuberculosis treated with linezolid, and to provide reference for clinical rational use of drugs.Methods:A total of 189 patients with multidrug-resistant pulmonary tuberculosis who were admitted to Hunan Chest Hospital between June 2019 and June 2020 were retrospectively included, and were divided into the linezolid group and the control group. The control group was given a standardized anti-tuberculosis treatment without linezolid, and the linezolid group was given linezolid in addition to standardized regimens. The occurrences of hematological toxicity, peripheral neuritis, optic neuritis and other adverse reactions in the two groups after anti-tuberculosis treatment were recorded. The risk factors for adverse reactions of linezolid were analyzed. Statistical analysis was performed using independent samples t test and chi-square test, and logistic regression was used to analyze the risk factors for adverse reactions of linezolid. Results:A total of 189 patients with MDR-TB were included in this study, including 108 in the linezolid group and 81 in the control group. There were no significant differences in baseline characteristics between the linezolid and control groups. The frequencies of leukopenia, anemia, thrombocytopenia, peripheral neuritis and optic neuritis in the linezolid group were 20.4%(22/108), 47.2%(51/108), 21.3%(23/108), 20.4%(22/108) and 13.9%(15/108), respectively, which were all significantly higher than those in the control group (8.6%(7/81), 27.2%(22/81), 9.9%(8/81), 1.2%(1/81) and 4.9%(4/81), respectively), and the differences were all statistically significant ( χ2=4.90, 7.86, 4.40, 15.86 and 4.10, respectively, all P<0.050). Patients older than 45 years of age was independent risk factor for leukopenia (odds ratio ( OR)=3.08, 95% confidence interval ( CI) 1.03 to 9.25, P<0.050) and thrombocytopenia ( OR=2.41, 95% CI 1.09 to 5.35, P<0.050) after linezolid administration. The higher value of white blood cell at baseline ( OR=0.48, 95% CI 0.30 to 0.76, P=0.002) was an independent protective factor for leukopenia associated with linezolid. Conclusions:Pancytopenia, peripheral neuritis and optic neuritis are prone to appear when linezolid is used to treat patients with multidrug-resistant pulmonary tuberculosis. In clinical practice, closely monitoring the adverse reactions during the use of linezolid for anti-tuberculosis treatment is needed.
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The aim of this study is to investigate the anti-inflammatory effect of the adenosine derivative N6-(3-hydroxylaniline) adenosine (WS070117M1) on cigarette smoke plus LPS (lipopolysaccharide)-induced chronic obstructive pulmonary disease (COPD) in mice and its mechanism. COPD model was established by exposing male BALB/c mice to cigarette smoke and challenged with LPS inhalation. Supernatants of bronchoalveolar lavage fluid (BALF) were harvested and IL-1β, IL-6, IL-8 and TGF-β1 levels were measured by ELISA (enzyme-linked immunesorbent assay). The number of total white blood cells and neutrophils in bronchoalveolar lavage fluid was counted separately. Lung tissue was stained with Mayer 's hematoxylin and eosin for histopathologic examination. pAMPKa protein expression and distribution of lung tissue were analyzed by immunohistochemistry method. In vitro, levels of AMPKα phosphorylation in phorbol-12- myristate-13-acetate (PMA) differentiated THP-1 cells was detected by immunohistochemistry, IL-8 level in supernatants of cigarette smoke condensate stimulating PMA differentiated THP-1 cells was measured by ELISA. The results showed that WS070117M1 treatment significantly activated AMPKa in the lung tissue. It also resulted in down regulation of IL-1β, IL-6, IL-8 and TGF-β1 levels in bronchoalveolar lavage fluid and IL-8 level in cigarette smoke condensate stimulating PMA differentiated THP-1 cells. In addition, WS070117M1 could inhibit the recruitment of total white blood cells and neutrophils. These results suggest that WS070117M1 may alleviate the airway inflammation by activating AMPK in the lung tissue.
Subject(s)
Animals , Humans , Male , Mice , AMP-Activated Protein Kinases , Metabolism , Adenosine , Bronchoalveolar Lavage Fluid , Cell Line, Tumor , Disease Models, Animal , Inflammation , Drug Therapy , Interleukin-1beta , Metabolism , Interleukin-6 , Metabolism , Interleukin-8 , Metabolism , Leukocyte Count , Lipopolysaccharides , Mice, Inbred BALB C , Neutrophils , Cell Biology , Pulmonary Disease, Chronic Obstructive , Drug Therapy , Smoke , Nicotiana , Transforming Growth Factor beta1 , MetabolismABSTRACT
This study is to investigate the effect of Vam3, a dimeric derivative of resveratrol, on SNP-induced apoptosis and its potential mechanism in rat articular chondrocytes. Isolated rat articular chondrocytes were treated with sodium nitroprusside (SNP), a NO donor, to induce apoptosis. Apoptosis percentage was evaluated by Annexin V-PI and nucleus fracture was examined by DAPI staining. Level of intracellular reactive oxygen species (ROS) was detected using 2, 7'-dichlorofluorescin diacetate (DCFH-DA) as a fluorescence probe by fluorescence microplate reader. The change in mitochondrial membrane potential was detected by TMRE staining. Expressions of SIRT1, acetylated p53 (ac-p53), cleaved caspase 9 and cleaved caspase 3 were determined by Western blotting. It showed that Vam3 up to 10 micromol x L(-1) could significantly reduce SNP-induced rat articular chondrocytes apoptosis (P < 0.01) and nucleus fracture, inhibit the increase of intracellular ROS level (P < 0.01) and reverse the decrease in mitochondrial membrane potential (P < 0.01). Simultaneously, Vam3 could upregulate the expression of SIRT1, deacetylate p53, and inhibit the cleavage of caspase 9 and caspase 3 (P < 0.01) of rat articular chondrocytes exposed to SNP. This study indicates Vam3 could protect rat articular chondrocytes against SNP-induced apoptosis, perhaps through the upregulation of SIRT1 and deacetylation of p53.
Subject(s)
Animals , Male , Rats , Apoptosis , Arabidopsis Proteins , Pharmacology , Cartilage, Articular , Cell Biology , Caspase 3 , Metabolism , Caspase 9 , Metabolism , Cells, Cultured , Chondrocytes , Cell Biology , Metabolism , Membrane Potential, Mitochondrial , Nitric Oxide Donors , Pharmacology , Nitroprusside , Pharmacology , Qa-SNARE Proteins , Pharmacology , Rats, Wistar , Reactive Oxygen Species , Metabolism , Sirtuin 1 , Metabolism , Tumor Suppressor Protein p53 , MetabolismABSTRACT
Objective To construct luciferase reporter vector containing full-length high-mobility group box 1 ( HMGB1, GenBank NM-010439) promoter for the screening of medicine. Methods The full-length HMGB1 promoter was amplified by polymerase chain reaction ( PCR) , and then was inserted into GV238 vector to construct plasmid GV238-HMGB1-P-Luc. GV238-HMGB1-P-Luc combined with internal reference plasmid pRL was co-transfected into Hela cells ( GV238-HMGB1-P-Luc group, which served as positive control group) . Plasmid pGL3-basic combined with pRL was co-transfected into Hela cells (pGL3-basic group, which served as negative control group) . Additionally, lipopolysaccharides ( LPS, 0.2 μg/mL) was used as the activator for the positive control group (LPS group), and then sodium butyrate (SB, 10 mmol/L) was used as the inhibitor for LPS group ( SB group) . At the end of experiment hour 24, luciferase activity was detected. Results The results of digestion, amplification, sequencing and identification showed that the full length of HMGB1 promoter was 2 140 bp, and the DNA sequence was correct, without mutation. Luciferase activity in GV238-HMGB1-P-Luc group was increased as compared with that of the pGL3-basic group ( P<0.05) . Luciferase activity in the LPS group was increased ( P<0.01, compared with that of GV238-HMGB1-P-Luc group) , and then was decreased after the administration of SB ( P<0.01, compared with that of the LPS group) . Conclusion A model of luciferase reporter vector containing HMGB1 promoter has been successfully constructed. Its activity can be increased by LPS, and then is in hibited by SB. The model can be used for further screening of medicine with the activities of regulating HMGB1 promoter.
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<p><b>OBJECTIVE</b>To identify the anti-inflammatory effects of artificial musk aqueous extract(AME)on lipopolysaccharide-stimulated cytokines secreted or released by RAW264.7 cells.</p><p><b>METHODS</b>Cytokines including interleukin(IL)-6,IL-10,and tumor necrosis factor Α were determined using cytokine enzyme-linked immunosorbent assay kits.</p><p><b>RESULT</b>Compared with model group,the levels of major cytokines such as tumor necrosis factor Α,IL-6,and IL-10 significantly decreased in different AME groups in a dose-dependent manner.</p><p><b>CONCLUSION</b>In lipopolysaccharide-stimulated RAW264.7 macrophages,AME can remarkably inhibit the release of inflammatory cytokines and thus exerts its anti-inflammatory effects.</p>
Subject(s)
Animals , Anti-Inflammatory Agents , Pharmacology , Cell Line, Tumor , Cytokines , Metabolism , Enzyme-Linked Immunosorbent Assay , Fatty Acids, Monounsaturated , Pharmacology , Inflammation Mediators , Metabolism , Interleukin-6 , Metabolism , Lipopolysaccharides , Macrophages , Tumor Necrosis Factor-alpha , MetabolismABSTRACT
Objective To understand the morbidity of human brucellosis in Wulanchabu City of Inner Mongolia in order to provide a basis for development of prevention and control measures.Methods According to the requirements in Baseline Survey Programme of Human Brucellosis in Inner Mongolia Autonomous Regionbetween November and December in 2010,stratified cluster sampling method was used to selected three townships according to the conditions of brucellosis(mild,moderate and serious) in 11 flags(cities,counties,districts) of the city.Three villages were extracted from each township.There were at least 200 persons aged 10 and older were investigated in every township.At least 600 people were investigated in every flag(city,county,district).Respondents were investigated about their awareness rate of basic knowledge about brucellosis,risk factors and common sense of prevention and treatment of the disease by using health education questionnaire.Based on the principle of informed consent,we collected respondents venous blood for preliminary screening using Hu red tablets.Brucellosis was confirmed with standard tube agglutination test and positive result was confirmed if 1:100 antibody concentration was two + or more.Prevalence,false negative rate as well as different age,gender,occupational incidence was calculated based on the network reported results of brucellosis in 33 townships of Wulanchabu in 2010.Results We distributed 6998 questionnaires and 6763 questionnaires were effective.The witting rate of basic knowledge about brucellosis was 57.99%(15 687/27 052); the witting rate of risk factors about brucellosis was 44.33% (29 978/67 630); the witting rate for prevention and control of brucellosis was 41.66%(28 176/67 630),and total witting rate was 45.49%(73 841/162 312).The morbidity of brucellosis in Wulanchabu City was 91.39/10 000 (785/85 894) in 2010.Five hundred and ninety-one were serologically positive and the infection rate was 8.48% (591/69 972).Nine hundred and three cases of patients were diagnosed with brucellosis and the prevalence rate of brucellosis was 105.13/10 000 (903/85 894).Missing report 377 cases,and the false negative rate was 48.03% (377/785) in 2010.Men infection rate was 71.07%(420/3755) and women infection rate was 28.93%(171/3217).The infection rate[97.63%(577/591)] of people aged 31 and older was significantly higher than that [2.37%(14/591)] of the people aged 30 and younger.Infection rate of people engaged in aquaculture was 8.61% (582/669).The infection rate of people working in livestock processing industry was 2.91% (2/103).The infection rate of people working in animal by-product circulation was 2.85% (2/70).The Infection rate of people working in other industries was 4.59%(5/109).Conclusions In Wulanchabu City,the morbidity of brucellosis and missing report rate are both high.The infection rate of people engaged in aquaculture is high and man morbidity is high.The awareness rate about prevention and treatment knowledge of brucellosis is low.We should carry out health education to inhabitants in endemic areas to improve their self-protection awareness and reduce the incidence of brucellosis.
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Human embryonic stem cells (hESCs) are pluripotent cells that have the ability of unlimited self-renewal and can be differentiated into different cell lineages, including neural stem (NS) cells. Diverse regulatory signaling pathways of neural stem cells differentiation have been discovered, and this will be of great benefit to uncover the mechanisms of neuronal differentiation in vivo and in vitro. However, the limitations of hESCs resource along with the religious and ethical concerns impede the progress of ESCs application. Therefore, the induced pluripotent stem cells (iPSCs) via somatic cell reprogramming have opened up another new territory for regenerative medicine. iPSCs now can be derived from a number of lineages of cells, and are able to differentiate into certain cell types, including neurons. Patient-specifi c iPSCs are being used in human neurodegenerative disease modeling and drug screening. Furthermore, with the development of somatic direct reprogramming or lineage reprogramming technique, a more effective approach for regenerative medicine could become a complement for iPSCs.
Subject(s)
Humans , Cell Differentiation , Cell Lineage , Cell Transdifferentiation , Cellular Reprogramming , Embryonic Stem Cells , Cell Biology , Induced Pluripotent Stem Cells , Cell Biology , Transplantation , Neural Stem Cells , Cell Biology , Transplantation , Neurodegenerative Diseases , Therapeutics , Regenerative Medicine , Transcription Factors , Genetics , MetabolismABSTRACT
ObjectiveTo investigate the injury mechanism,clinical characteristics and surgical treatments of Segond fracture combined with anterior cruciate ligament (ACL) injury.MethodsNine patients suffering from Segond fracture combined with ACL injury were treated between January 2008 and December 2010.All the patients revealed ACL and medial collateral ligament (MCL) breakage under arthroscopy.Furthermore,one patient was associated with lateral collateral ligament (LCL) breakage and medial meniscus injury,four with medial meniscus tear and two with lateral meniscus tear.All the patients underwent arthroscopic tendon allotransplantation,ACL reconstruction and MCL repair.Besides,synchronous LCL reconstruction was performed in one patient,meniscus suture in three and meniscus plasty in four.Six patients with large Segond fracture fragments were fixed with two hollow lag crews and three with relatively small fracture fragments fixed with one hollow lag crew.ResultsThe mean followup period was 12 months,which showed average postoperative Lysholm score of 59 points and satisfactory clinical outcome.ConclusionsSegond fracture is often combined with ACL injury and is predictive for ACL injury.In ACL reconstruction,large Segond fracture blocks should be reduced and fixed and the combined injuries also should be treated in the same period.
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The aim of the present study is to investigate the effects of Vam3 which is one of the dihydroxystilbene compounds on expressions of ICAM-1 in the lungs of OVA-induced asthmatic mice and the mechanisms of anti-airway inflammation. Balb/c mice were challenged with OVA inhalation. Lung tissues were stained with Mayer's hematoxylin and eosin for histopathologic examination. The expression of ICAM-1 in the lungs of mice was analyzed by Western blotting and immunohistochemistry method. The NF-kappaB activities were detected by NF-kappaB-luc reporter genetic transient transfection method. The activities of MMP-9 induced by LPS, TNF-alpha and PMA in THP-1 cells were determined by gelatin zymography method. The results showed that Vam3 could inhibit the expression of ICAM-1 in the OVA-induced mouse model. In addition, Vam3 could significantly suppress the activities of NF-kappaB in A549 cells and MMP-9 in THP-1 cells induced by LPS, TNF-alpha and PMA. These results suggested that Vam3 could alleviate the asthmatic inflammation by decreasing ICAM-1 expression in asthmatic mice, down regulating NF-kappaB and MMP-9 activities. Compound Vam3 showed inhibitory effects on inflammatory signal pathways involved in asthma.
Subject(s)
Animals , Humans , Male , Mice , Anti-Asthmatic Agents , Pharmacology , Anti-Inflammatory Agents , Pharmacology , Asthma , Metabolism , Benzofurans , Pharmacology , Cell Line, Tumor , Inflammation , Metabolism , Intercellular Adhesion Molecule-1 , Metabolism , Leukemia, Myeloid , Metabolism , Pathology , Lung , Metabolism , Pathology , Lung Neoplasms , Metabolism , Pathology , Matrix Metalloproteinase 9 , Metabolism , Mice, Inbred BALB C , NF-kappa B , Metabolism , Ovalbumin , Stilbenes , PharmacologyABSTRACT
Objective To observe the neurological recovery and endogenous neural stem cell proliferation in rats with spinal cord injury after acupuncture on Governing Vessel and Jiaji (Ex-B2) acupoints. Methods Forty-eight adult SD rats with severe spinal cord injury at the T10 level induced with the method of Allen were randomly divided into two groups (A and B), and each was further randomized into 4 subgroups. In group A, acupuncture was performed once daily on the Governing Vessel and Jiaji (Ex-B2) points, which was not performed in group B. Bromodeoxyuridine (BrdU) was administered intraperitoneally twice daily 3 days prior to heart perfusion for labeling the proliferating endogenous neural stem cells. Open field and inclined plane tests were performed to test the function of the rear limbs of the rats at 1, 14, 30, 60, 90 days after the surgery. The 4 subgroups of rats were sacrificed on days 14, 30, 60 and 90 after the surgery, and the number of BrdU-positive cells and their distribution in the spinal cord was observed in each subgroup using immunohistochemistry with anti-BrdU. Results The rats in group A showed significantly improved neurological function than those in group B (P<0.05). The number of BrdU-positive cells in group A was significantly different from that in group B at each of the time points (P<0.05). Conclusion Acupuncture on the Governing Vessel and Jiaji (Ex-B2) acupoints can promote the functional recovery of the rear limbs and induce the proliferation of endogenous neural stem ceils in situ in rats following spinal cord injury.
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@#ObjectiveTo evaluate the assistant effct of electroacupuncture on acute incomplete spinal cord injury treated with routine therapy.Methods9 cases who accepted routine therapy, including operation and medicine, were in control group, while other 7 cases who accepted electroacupuncture other than routine therapy were in treating group.ResultsThere were 2 cases were effective, 4 cases were improved and 3 cases were not improved in control group, while 6 cases were clinical recovery, 1 case was effective in treating group.ConclusionElectroacupuncture can improve the effect of routine therapy on acute incomplete spinal cord injury.
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<p><b>AIM</b>To investigate the regulatory effects of various anti-inflammatory drugs on both endogenous and TNFalpha-induced NF-kappaB activation as well as the relative biological activity.</p><p><b>METHODS</b>HEK293 cells were cultured in 96-well plate and 6-well plate, treated with meloxicam, indomethacin, dexamethasone and hydrocortisone, without or with 10 ng.mL(-1) TNFalpha for 24 hours. Then cell proliferation was measured by MTT and cell apoptosis was analyzed by pI stain-flow cytometry. HEK293/ kappaB-luc cells transfected stably with pElam-kappaB-luc vector, were cultured in 96-well plate and treated as above. Equal amounts of cell lysates were tested for luciferase activity which represents NF-kappaB activation.</p><p><b>RESULTS</b>Endogenous NF-kappaB activation was present in HEK293 cells and its level can be increased about 2 times by 10 ng.mL(-1) TNFalpha-induction. Dexamethasone (1 x 10(-8) mol.L(-1)) and meloxicam (1 x 10(-7) - 1 x 10(-6) mol.L(-1)) can decrease both endogenous and TNFalpha-induced NF-kappaB activation. Hydrocortisone (1 x 10(-9) mol.L(-1)) increases endogenous NF-kappaB activation but decreases TNFalpha-induced one significantly. No influence of indomethacin on endogenous NF-kappaB activation was observed. However, its influence on TNFalpha-induced NF-kappaB activation is needed for further study. Cell apoptosis was observed after treatment with TNFalpha and 1 x 10(-8), 1 x 10(-6) mol.L(-1) dexamethasone and 1 x 10(-7) mol.L(-1) indomethacin, or only with dexamethasone. No significant effect of these anti-inflammatory drugs on cell proliferation was observed.</p><p><b>CONCLUSION</b>Various anti-inflammatory drugs differ in their ability to regulate NF-kappaB activation in HEK293 cells, which indicates that NF-kappaB activation might be a potential useful target to study mechanism and for drug screening.</p>
Subject(s)
Humans , Anti-Inflammatory Agents , Pharmacology , Apoptosis , Cell Line , Cell Proliferation , Dexamethasone , Pharmacology , Embryo, Mammalian , Hydrocortisone , Pharmacology , Indomethacin , Pharmacology , Kidney , Cell Biology , Metabolism , NF-kappa B , Metabolism , Thiazines , Pharmacology , Thiazoles , PharmacologyABSTRACT
@# 目的观察神经外科与针刺联合治疗急性脊髓不完全损伤的疗效。方法神经外科治疗组根据指征确定是否进行手术,药物治疗均给予激素、脱水、抗去甲肾上腺素类药物、神经营养药物,高压氧。神经外科与针刺联合治疗组除上述神经外科治疗外,采用针刺治疗,针刺处方:电针刺激夹脊穴,根据不同辨证配合远端取穴。结果神经外科治疗组9例,持续治疗 3—6个月,出院后随访6个月,6例好转,肌力有所改善,最好者可达到肌力IV—IV+级,3例无效,甚至退步,瘫痪进一步加重。神经外科与针刺联合治疗组病人5例,经针刺及电针治疗10—80天时间后,4例临床治愈,1例经针刺治疗好转后,因转入骨科手术治疗腰椎压缩性骨折时脱离针刺治疗。结论神经外科与针刺联合治疗急性脊髓损伤效果好,并能抑制脊髓损伤的进一步恶化。
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@#目的观察以针灸为主结合按摩、康复训练等方法治疗儿童交通性脑积水的效果。方法 26例儿童交通性脑积水患者接受针灸、按摩、康复训练及引导式教育。结果26例患者,治愈 5例(随访4例)、显效4例、有效10例、无效7例,总有效率73.07%。结论以针灸为主结合康复训练等方法可改善儿童交通性脑积水患者的症状。
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<p><b>AIM</b>To study the effects of indomethacin on interleukin-6 (IL-6) expression stimulated with lipopolysaccharide (LPS) in rheumatoid arthritic patients' synoviocyte.</p><p><b>METHODS</b>Fibroblast-like cells (FLS) from rheumatoid arthritic patients' joint tissue were cultured for 24 h and incubated 24 h with LPS (1 mg.L-1) or the supernatant of U937 cells stimulated by LPS (1 mg.L-1). After indomethacin or dexamethasone added into the supernatant of U937 cells, FLS was incubated with the super natant for 24 h. The expression of IL-6 protein was detected by radioimmunoassay. The mRNA expression of IL-6 was accessed by RT-PCR.</p><p><b>RESULTS</b>LPS did not obviously affect the growth of FLS, and the protein secretion and mRNA expression of IL-6 were not changed in FLS treated with LPS. The IL-6 secretion and IL-6 mRNA expression were significantly increased in FLS cultured with the supernatant from U937 cell treated with LPS. Indomethacin at concentrations of 1 x 10(-7)-1 x 10(-5) mol.L-1 obviously inhibited the protein secretion and mRNA expression of IL-6 in FLS cultured with the supernatant from U937 cell stimulated with LPS, and the inhibitory effects increased as the concentrations of indomethacin increased.</p><p><b>CONCLUSION</b>Indomethacin can inhibit the increase of IL-6 expression caused by supernatant of U937 cells stimulated with LPS in FLS.</p>
Subject(s)
Humans , Anti-Inflammatory Agents, Non-Steroidal , Pharmacology , Arthritis, Rheumatoid , Metabolism , Pathology , Cells, Cultured , Fibroblasts , Metabolism , Pathology , Indomethacin , Pharmacology , Interleukin-6 , Genetics , Lipopolysaccharides , Pharmacology , RNA, Messenger , Genetics , Synovial Membrane , Metabolism , Pathology , U937 CellsABSTRACT
<p><b>AIM</b>To investigate the expression of matrix metalloproteinase-9 (MMP-9) in mouse ears induced with croton oil and the inhibitory effect of dexamethasone, indomethacin and resveratrol on MMP-9 expression, and further explore the relationship between anti-inflammation and MMP-9 inhibition of these three medicines.</p><p><b>METHODS</b>Immuno-histochemistry was used to detect the expression of MMP-9 in mouse ears. Expression of MMP-9 in U937 cells was analyzed by gelatin zymography.</p><p><b>RESULTS</b>Mouse ear edema induced with croton oil was inhibited significantly by dexamethasone and indomethacin at the dose of 10 mg.kg-1 and resveratrol at 50 mg.kg-1 administered subcutaneously. The inhibitory rate was 76.2% (P < 0.001), 56.7% (P < 0.001) and 36.9% (P < 0.001) respectively. The MMP-9 expression increased in mouse ears induced with croton oil and inhibited by dexamethasone, indomethacin and resveratrol at above doses. Gelatin zymography results showed that MMP-9 expression in U937 cells increased significantly after exposed to PMA at 1 x 10(-8) mol.L-1 (P < 0.001); MMP-9 expression induced with phorbol myristate acetate(PMA) was inhibited by dexamethasone at 1 x 10(-9), 1 x 10(-7) and 1 x 10(-5) mol.L-1, indomethacin at 1 x 10(-6) and 1 x 10(-5) mol.L-1 and resveratrol at 1 x 10(-6) and 1 x 10(-5) mol.L-1.</p><p><b>CONCLUSION</b>The inhibition of MMP-9 expression may be one of the anti-inflammatory mechanisms of dexamethasone, indomethacin and resveratrol.</p>
Subject(s)
Animals , Humans , Male , Mice , Anti-Inflammatory Agents , Pharmacology , Anti-Inflammatory Agents, Non-Steroidal , Pharmacology , Croton Oil , Dexamethasone , Pharmacology , Ear Diseases , Metabolism , Edema , Metabolism , Indomethacin , Pharmacology , Matrix Metalloproteinase 9 , Metabolism , Matrix Metalloproteinase Inhibitors , Mice, Inbred ICR , Random Allocation , Stilbenes , Pharmacology , U937 Cells , MetabolismABSTRACT
Objective To investigate the influence of acupuncture on Nestin expression in the cerebral cor- tex of hypoxia-ischemic neonatal rats.Methods A total of 72 Sprague-Dawley(SD)rats aged 7 days were random- ly divided into three groups:A normal group(n=24),the hypoxic-ischemic encepbalopathy(HIE)group(n=24), and an acupuncture+HIE group(n=24).The rats were sacrificed at time points including 3d,7d,14d and 28d af- ter insult,their brains were removed and sections were made.Any nerve stem cells(NSCs)in the cerebral cortex were detected using immunohistochemical staining of Nestin.Results Nestin-positive cells were found in the cere- bral cortex in the normal neonatal SD rats early after birth.After HI insult,the Nestin-positive cells had increased in the injured areas of the cortex and in contralateral mirror areas,especially around the injured areas.Peak Nestin ex- pression was 3 days after insult.In the acupuncture+HIE group,Nestin positive cells were significantly increased when compared with that in the HIE group,the peak was postponed,and the peak was longer than in the HIE group. The Nestin positive cells decreased,were seldom seen,and were not different among three groups 28 days after the HI insult.Conclusions Endogenous neural stem cells in the cerebral cortex were increased by acupuncture in hy- poxia-ischemic in neonatal rats,and acupuncture made the peak of Nestin expression longer.
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Objective To investigate the effects of acupuncture on gene expression profile of neurotrophin and its receptors in cerebral cortex of neonatal rats after cerebral hypoxic-isehemic injury,and to explore the molecu- lar mechanism of acupuncture in treatment of neonatal hypoxic-ischemic encephalopathy.Methods The model of cerebral hypoxic-ischemic injury was established with 10 neonatal Sprague-Dawley(SD)rats,who were subjected to acupuncture once daily for 14 days.The animals were sacrificed on the next day of the last acupuncture and their brain cortex was sampled for examination of gene expression,using GEArray Q series neurotrophin and receptors gene array.Results After 14 days of acupuncture,it was found that 48 genes(50% of total genes on the microarray) were expressed differently between the two groups,of which 40 genes(83.3% of differently expressed genes),such as those of the brain-derived neurotrophic factor(BDNF),ciliary neurotrophic factor(CNTF),ciliary neurotrophic factor receptor(CNTFR),basic fibroblast growth factor(bFGF)and fibroblast growth factor receptor type 1 (FGFR1)were up-regulated,and 8 genes(16.7% of differently expressed genes),such as genes of neuregulin-1 (Nrg1),neuregulin-4(Nrg4)and tyrosine kinase C(TrkC)were down-regulated.Conclusion Acupuncture can regulate the expression of various genes of neurotrophin and receptors in cerebral cortex of neonatal rats after cerebral hypoxic-ischemic injury,which might be the mechanism of acupuncture facilitating the recovery of the rats from hy- poxic-ischemic encephalopathy.