RESUMEN
OBJECTIVE：To systematically evaluate the efficacy and safety of linezolid （LZD）combined with routine anti- tuberculosis drugs in the treatment of tuberculous meningitis （TBM），so as to provide evidence-based reference for clinical medi- cation. METHODS ：Retireved from PubMed ，Cochrane Library ，Embase，CNKI and Wanfang database ，randomized controlled trials（RCT）of LZD combined with routine anti-tuberculosis drugs （trial group ）versus routine anti-tuberculosis drugs （control group）were collected from the inception to Jan. 2020. After literature screening and data extraction ， the quality of the included literature were evaluated with bias risk assessment tool recommended by Cochrane system evaluator handbook 5.2. Meta-analysis was conducted by using Rev Man 5.3 software，and sensitivity analysis and publication bias analysis were performed. RESULTS ： Totally 9 RCTs involving 602 patients were included. Meta-analysis showed that total response rate [OR ＝4.05，95％CI（2.26，7.26）， P＜0.000 01]， changes of protein content of cerebrospinal fluid [MD ＝0.48，95％CI（0.20，0.77），P＝0.000 8]，changes of white blood cells count of cerebrospinal fluid [MD ＝44.43，95％CI（20.06，68.81），P＝0.000 4]，changes of cerebrospinal fluid glucose/ synchronous blood glucose [MD ＝0.09，95％CI（0.05，0.14），P＜0.000 1] of trial group were significantly higher than those of control group. There was no statistical significance in the changes of chloride content of cerebrospinal fluid [MD ＝8.08，95％CI（－0.64， 16.80），P＝0.07] and the incidence of ADR [OR ＝1.34，95％CI（0.57，3.11），P＝0.50] between 2 groups. The results of sensitivity analysis showed that there were significant differences comparison with before exclusion when the change of protein content in cerebrospinal fluid and the change of glucose/synchronous blood glucose in cerebrospinal fluid were taken as indexes ，and there was no significant difference comparison with before exclusion when the changes of white blood cell count and chloride content in cerebrospinal fluid were taken as indexes. The results of publication bias analysis showed that there was a certain publication bias in this study. CONCLUSIONS ：LZD combined with conventional anti-tuber culosis drugs is effective and safe for TBM. Because the inconsistent results of sensitivity analysis and publication bias exists in publication bias analysis ，the conclusions need to be further confirmed by more large sample and multi-center studies.
RESUMEN
Rheumatoid Arthritis is a kind of chronic autoimmune diseases mainly involving joint, which is characterized by systemic inflammatory response.Studies have shown that Rheumatoid arthritis patients showed associated antineutrophil cytoplasmic antibody (ANCA) and inflammatory cytokines such as interleukin (IL) , tumor necrosis factor (TNF) increased, the positive of ANCA and the increase of IL-1, IL-6, TNF-αare especially seen in the Rheumatoid arthritis patients who have inflammatory reaction, and which are roughly equal to the articular synovitis pathological mechanism of wind dampmess heat accumulation pattern in the traditional Chinese medicine.The treatment for Rheumatoid arthritis patients, Western treatment is use the methotrexate (MTX) as basic drugs, combined with other drugs to control the positive of ANCA and the higher of IL-1, IL-6, TNF-α.And combining traditional Chinese medicine treatment, the effect is not only at to increase Western effection but also be able to reduce the side effects of Western medicine.Therefore, the research of combined rheumatoid factor ANCA, IL-1, IL-6, TNF-αdetection is benefit to diagnosing rheumatoid arthritis.
RESUMEN
Objective To investigate the effect of norepinephrine (NE) on the proliferation and migration capacity of endo‐thelial progenitor cells (EPCs) ,and bone marrow mobilization and to analyze its molecular mechanism .Methods The 8‐week old C57 mice were taken and randomly divided into 3 groups ,5 cases in each group :the blank control group(subcutaneous injection of normal saline without operaion) ,model group(subcutaneous injection of normal saline and ischemia in left lower extremity ) and NE group(subcutaneous injection of NE 100μmol/100 μL and ischemia in left lower extremity) .The limb ischemia model was prepared by adopting the femoral arterial ligation in mouse left lower extremity ,then NE was continuously pumped by the micro‐osmotic pump .The EPCs contents from bone marrow ,peripheral blood and spleen were assayed with the flow cytometric analyzer ;human peripheral blood EPCs were cultured and stimulated by NE .The proliferation and migration capacity ,and the activation situation of Akt and eNOS signal pathway were detected .Results NE could promote the mobilization of bone marrow EPCs in limb ischemia mice ,increased the EPCs quantity of peripheral blood and spleen ,comparing the NE group with the model group ,the EPCs quantity was increased for bone marrow [(3 .271 ± 0 .772)% vs .(1 .320 ± 0 .256)% ] ,peripheral circulation[(0 .261 ± 0 .041)% vs .(0 .110 ± 0 .028)% ] and spleen[(4 .671 ± 0 .345)% vs .(1 .880 ± 0 .0 .381)% ] ,the differences were statistically significant (P<0 .01) .NE could promote the proliferation and migration capacity ,moreover could activate the Akt‐eNOS signal pathway in EPCs with a dose dependent manner .Conclusion NE could promote the proliferation and migration of EPCs and mouse bone marrow mobilization via the Akt‐eNOS signal pathway .
RESUMEN
Objective: To investigate the role of aldehyde dehydrogenase-2 (ALDH-2) for regulating human endothelial progenitor cells (EPCs) oxidative stress reaction and its mechanism. Methods: Human EPCs were isolated from peripheral blood of healthy adults and the cells were cultured in 4 groups:①Blank control group,②Alda-1 group, the cells were treated by 1μmol/L Alda-1, a speciifc activator of ALDH-2,③tBHP (10μg/ml) group and④Alda-1 pretreatment+tBHP group. EPCs reactive oxygen species (ROS) levels were evaluated by DCFH-DA staining, mitochondrial membrane potentials were detected by JC-1 method, migration capacity was measured by transwell chamber method and the activation of p38 signal pathway was examined by Western blot analysis. Results: Compared with Blank control group, ROS levels in tBHP group and Alda-1 pretreatment+tBHP group were (441.7 ± 24.8) % and (237.4 ± 12.0) %, allP<0.05. In Blank control group, tBHP group and Alda-1 pretreatment+tBHP group, the proportion of EPCs lost their mitochondrial membrane potentials were (5.7 ± 2.1) %, (81.7 ± 3.7) % and (37.4 ± 3.2) % respectively, allP<0.05; the number of EPCs migration were (108 ± 9)/HP, (22 ± 4)/HP and (67 ± 7)/HP respectively, allP<0.05. Compared with Blank control group, the activation of p38 signal pathway increased to (259.1 ± 7.7) % in tBHP group, while it was reduced to (186.4 ± 8.0) % in Alda-1 pretreatment+tBHP group. Conclusion: ALDH-2 could reduce ROS level in human EPCs, it may decrease mitochondrial membrane damage, protect migration which might be related to p38 signal pathway.
RESUMEN
Objective To investigate the effect of astaxanthin( ASX)on endothelial progenitor cells( EPCs)injury induced by oxidative stress in vitro and to explore its underlying mechanism. Methods Cultured EPCs isolated from peripheral blood were randomly divided into 5 groups:normal control,model group[ tert-butyl hydroperoxide( tBHP)100μmol·L-1 ],and ASX+tBHPgroups(thecellswerepreconditionedwithASX0.1,1.0,and10.0nmol·L-1,respectively).Thecellviabilitywas measured by MTT method. The level of reactive oxygen species( ROS)was determined by DCFH-DA method. The changes of mitochondrial membrane potential( MMP)and apoptosis ratio were detected by JC-1 method and DAPI method,respectively. caspase-3 activity changes of EPCs were detected. Results The cell viability of EPCs was improved with the increasing concentration of ASX. Compared with the model group[(48. 5±4. 3)%],0. 1,1. 0,10. 0 nmol·L-1 ASX significantly increased the cell viabilities[(57. 6±8. 2)%,(77. 6±7. 5)%,and(85. 3±6. 1)%,P﹤0. 05]. The results of DAPI staining revealed that ASX pretreatment could significantly reduce the apoptotic rate of EPCs. The apoptotic rate of the model group was( 27. 8 ± 3. 2)%,while that of ASX+tBHP groups was[(20. 4±2. 9)%,(14. 9±1. 7)%,and(7. 8±0. 7)%,P﹤0. 05],respectively. The data from caspase-3 activity assay indicated that ASX precondition could also remarkably decrease the caspase-3 activity for EPCs. The caspase-3 activity of the model group was(0. 345±0. 018),while that of the ASX+tBHP group were[(0. 291± 0. 013),(0. 209±0. 004),and(0. 169±0. 013),P﹤0. 05],respectively. In addition,treatment with tBHP resulted in an increase of DCF fluorescence,while ASX precondition could decrease the DCF fluorescence,which suggested the accumulation of intercellular ROS for EPCs. Injury of michondrial membrane resulted in the loss of mitochondrial membrane potential( MMP). The MMP detected by JC-1 method revealed that compared with model group,pretreatment of ASX inversed the reduction of MMP. Conclusion Astaxanthin inhibits endothelial progenitor cell apoptosis induced by oxidative stress through inhibiting ROS production,improving the mitochondrial function and down-regulating caspase-3 activity.