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Objective:To explore the interventional effect of β-sitosterol on ovalbumin(OVA)-induced allergic asthma rats and its potential mechanism.Methods:SD male rats were randomly divided into normal group(CON),model group(M),positive drug dexamethasone group(DEX,0.075 mg/kg)and β-sitosterol group(Sit,50 mg/kg).A rat model of allergic asthma was estab-lished by intraperitoneal injection of OVA with aluminum hydrogen solution,and nebulized inhalation of OVA to stimulate.Rats were given intragastric administration 30 min before aerosol challenge,and after continuous administration for 7 days,the indicators of cough and asthma and tracheal phenol red excretion were detected.HE staining was used to observe pathological changes of lung tis-sue.Flow cytometry was used to detect reactive oxygen species(ROS)generation,apoptosis level and ratios of Th17 and Treg cells in peripheral blood.Biochemical method was used to detect contents of MDA,and activities of T-SOD and GSH-Px in rat lung tissues.ELISA was used to detect levels of Th17 and Treg-related cytokines(TNF-α,IL-4,IL-6,IL-17A,and IL-35).Results:Compared with model group,β-sitosterol significantly prolonged the incubation period of cough and gasp in rats with allergic asthma,reduced the frequency of cough and gasping,and promoted the excretion of phenol red in trachea;significantly reduced inflammatory infiltration in lung tissue of asthmatic rats;observably reduced MDA content in lung tissue,ROS of primary lung cell and apoptosis levels of asthmatic rats,increased the activities of T-SOD and GSH-Px;markedly reduced proportion of Th17 cells and levels of pro-inflammatory cyto-kines TNF-α,IL-4,IL-6 and IL-17A,increased proportion of Treg cells and levels of anti-inflammatory cytokine IL-35.Conclusion:β-sitosterol can ameliorate airway inflammation and oxidative damage in OVA-induced allergic asthmatic rats,and its mecha-nism may be related to the regulation of β-sitosterol on Th17/Treg immune imbalance and oxidative stress response.
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Objective To Analyze the expression profiles of LncRNAs and mRNAs in ovarian epithelial cancer cell lines by gene mi-croarray, and then provide experimental evidences for investigating the function of LncRNAs associated with ovarian cancer. Methods The differentially expressed LncRNAs and mRNAs in ovarian epithelial cancer cell lines, such as A2780, HO8910 and SKOV3, and ovarian epithelial cell line HOSEpiC were analyzed by gene microarray. The differentially expressed mRNAs were further performed the KEGG pathway enrichment analysis. The expression levels of six candidate LncRNAs, which had significant difference between the o-varian epithelial cancer cell line and the ovarian epithelial cell line, were further verified by qRT-PCR. Results There were 227 up-regulated LncRNAs and 483 down-regulated LncRNAs in A2780, HO8910 and SKOV3 cell lines. The differentially expressed mRNAs in A2780, HO8910 and SKOV3 cell lines were mainly enriched in the tumor-related pathways such as PI3K-AKT, mTOR and TNF-α( P<0.05) . The expression levels of PTPRG-AS1, CCNT2-AS1, XLOC 009869 and LINC01138 in ovarian epithelial cancer A2780, SKOV3 and OVCR3 cell lines were up-regulated (P<0.05), while those of RP11-252P19.2 and RP11-744I24.2 in ovarian epithelial cancer A2780, SKOV3, OVCR3 and 3AO cell lines were down-regulated ( P<0.05) . Conclusion The differentially expressed LncR-NAs and mRNAs in ovarian epithelial cancer cell lines may be obtained by gene microarray, and the differentially expressed mRNAs are associated with the tumor-related pathways such as PI3K-AKT, mTOR and TNF-α, which may provide new targets for the diagnosis and treatment of ovarian cancer.
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OBJECTIVE@#To determine the effect of p38 MAPK inhibitor (SB203580) on TNF-α -induced high mobility group protein B1 (HMGB1) expression in microglial cells. @*METHODS@#Microglial cells were treated with TNF-α (25 ng/mL, TNF-α group), TNF-α plus SB203580 (10 μmol/L, TNF-α+SB203580 group), SB203580 (SB203580 group) or serum-free medium (control group). After 16 h of incubation, the protein levels of p-p38 MAPK and HMGB1, and mRNA levels of HMGB1 were examined by ELISA, Western Blot and RT-PCR, respectively. @*RESULTS@#There was a significant increase in p-p38 MAPK and HMGB1 levels in TNF-α-treated microglia cells (P<0.01). The TNF-α-induced HMGB1 protein and mRNA expression was suppressed by SB203580. @*CONCLUSION@#TNF-α up-regulates HMGB1 expression in microglial cells through activation of the p38 MAPK pathway.
Subject(s)
Humans , Blotting, Western , HMGB1 Protein , Metabolism , Imidazoles , Pharmacology , MAP Kinase Signaling System , Microglia , Metabolism , Pyridines , Pharmacology , Tumor Necrosis Factor-alpha , Pharmacology , Up-Regulation , p38 Mitogen-Activated Protein Kinases , MetabolismABSTRACT
Objective To analyze the diagnostic values of ultrasonography and computed tomography (CT)for gallbladder adenomyomatosis. Methods The ultrasound and CT findings of 28 cases of pathologically confirmed gallbladder adenomyomatosis in our hospital were retrospectively analyzed.The diagnostic values of the two imaging tools for gallbladder adenomyomatosis were analyzed with the pathological diagnosis as the gold standard.Comparison of rates was made by chi-square test;multiple comparisons of rates were made by partition of chi-square.Results Before operation,among the 28 patients,15 were diagnosed with gallbladder adenomyomatosis by ultrasonography,and 9 were diagnosed by CT;the diag-nostic rate of CT was 32.14%,and the diagnostic rate of ultrasonography was 53.57%.The chi-square test showed no difference between the di-agnostic rates of ultrasonography and CT for gallbladder adenomyomatosis (χ2 =2.63,P=0.10>0.05).In addition,the statistical results showed no differences between the diagnostic rates of ultrasonography and CT for various types of gallbladder adenomyomatosis (segmental type:χ2 =0,P=0.11>0.0125;diffuse type:χ2 =2.57,P=1.00>0.0125;focal type:χ2 =1.42,P=0.23>0.0125).Conclusion CT and ultrasonography are two important imaging methods for the diagnosis of gallbladder adenomyomatosis.The detection rate of gallbladder adenomyomatosis can be in-creased through the combination of convex array probe and linear array probe in ultrasonography.
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Objective To study the changes in interleukin-32 (IL-32) in rats with Klebsiella bacillus pneumonia and approach its significance. Methods Seventy-two Sprague-Dawley(SD)rats were divide into control group,model group and experimental group by the method of random digits table,then the experimental group was subdivided into 4 hours and 1,3 and 5 days experimental subgroups(each n=6). The rat model of Klebsiella bacillus pneumonia was established by injection of 0.3 mL Klebsiella bacterial suspension into the trachea. Before the establishment of the model in the experimental group,IL-32 inhibitory agent,protease activated receptor-2(PAR2) was injected into the abdominal cavity. After model establishment,at different time points,blood was collected via tail vein to observe the changes in serum levels of IL-32,tumor necrosis factor-α(TNF-α),IL-6 and IL-8 in all the groups. The lungs were removed and stained with hematoxylin-eosin(HE)method to investigate the histopathological changes of the lung tissues under the light microscope. Results Compared to the control group, with the prolongation of time the levels of IL-32,TNF-α,IL-8 and IL-6 were increased gradually in the model group,and reached their peaks at 3 days〔IL-32(ng/L):84.40±28.24 vs. 18.57±3.86,t=5.544,P=0.002;TNF-α(ng/L):79.27±14.64 vs. 17.82±3.86, t=9.994, P=0.000;IL-8(ng/L):55.85±10.90 vs. 16.66±3.76,t=8.544, P=0.000;IL-6(ng/L):56.65±2.57 vs. 28.48±2.11,t=19.693,P=0.000〕;PAR2 could inhibit above indexes significantly,there was statistical difference at 3 days compared with the model group〔IL-32(ng/L):54.13±6.68 vs. 84.40±28.24,t=2.560,P=0.046;TNF-α(ng/L):49.12±3.56 vs. 79.27±14.64,t=4.901,P=0.003;IL-8 (ng/L):22.95±2.52 vs. 55.85±10.90,t=7.204,P=0.000;IL-6(ng/L):36.49±2.63 vs. 56.65±2.57,t=13.443, P=0.000〕. Under the light microscope,the inflammatory changes in the lung tissue in experimental group were milder than those in the model group. Conclusion As a pro-inflammatory cytokine,IL-32 can induce the production of TNF-α,IL-6 and IL-8,and the inhibition of IL-32 production may play a role in suppression of the development of Klebsiella bacillus pneumonia.