In order to improve the knowledge of clinicians in hypoxia of COPD during the night,the physiological changes of arterial oxygen and carbon dioxide during sleep in healthy population were investigated at first,and the features and state of oxygen deficiency during sleep in patients with COPD were analyzed.Furthermore,the possible mechanism,effect,predictor,diagnosis and therapy were explored.

Objective To investigate the medical effect of the ethanol extract of Acorus gramineus Sol.on arthritis of mice induced by collagen-Ⅱ,and explore the potential pharmacological mechanisms.Methods Arthritis mouse model was established by injection of admixture containing type Ⅱ collagen and Freund's complete adjuvant (FCA) in male BALB/c mice.Mice were divided into five groups:the normal control group (0.9% of sodium chloride solution),the model control group (0.9% of sodium chloride solution),tripterygium group (15 μg·kg-1 of tripterygium tablets), the high-dose of extract of Acorus gramineus Sol.group (60 mg·kg-1 extract of Acorus gramineus Sol.) and the low-dose of extract of Acorus gramineus Sol.group (15 mg·kg-1 extract of Acorus gramineus Sol.).Each group was administered once a day,lasting 21 days.During the experiment,ankles of all mice were measured at predetermined time.At the end of the experiment,blood of the mice was exsanguinated and centrifuged to get serum for measuring the levels of IL-1β,RF and TNF-α.Spleens of mice were dissected and weighed to calculate the spleen index.All arthritis ankles were dissected to make tissue section,and observed under microscope.Results Compared with the model control group,the perimeter of ankle joints of the high-dose of extract of Acorus gramineus Sol.group significantly changed 6 days after administration (P<0.05);That of the low-dose of extract of Acorus gramineus Sol.group significantly changed 12 days after administration (P<0.05);That of tripterygium group significantly changed 9 days after administration (P<0.05).As compared with the normal control group, the spleen index of the model control group was significantly different (P<0.01).As compared with the model control group,the spleen index of tripterygium group,high-dose and low-dose of extract of Acorus gramineus Sol.groups were significantly different (P<0.05).As compared with the normal control group,levels of IL-1β,RF and TNF-α of the model control group were significantly different (all P<0.01).As compared with the model control group,levels of IL-1β,RF and TNF-α of tripterygium group,high-dose and low-dose of extract of Acorus gramineus Sol.groups were significantly decreased.Conclusion Ethanol extracts of Acorus gramineus Sol.have significant therapeutic effect on arthritis mice.The anti-arthritic mechanism is associated with its ability to regulate levels of IL-1β,RF and TNF-α.

AIM: To study the effect of cigarette smoke extract (CSE) on adhesion and migration of human airway epithelial cells and it's mechanism. METHODS: After 24 h culture, the airway epithelial cells were treated with different concentrations of CSE. The rate of cell attachment and the velocity of cell migration were measured. The expression of FIP200 mRNA and protein were analyzed by RT-PCR and Western blotting. RESULTS: CSE inhibited the rate of cell attachment and the velocity of cell migration. Meanwhile CSE increased the expression level of FIP200 mRNA and FIP200 protein. The effects of CSE became more evident with increased concentration of CSE. Expression of FIP200 mRNA and FIP200 protein were positively correlated to the decreased rate of cell attachment and the velocity of cell migration. CONCLUSION: CSE inhibits the rate of cell attachment, the velocity of cell migration and increases the expression of FIP200.

The effect of cigarette smoke extract (CSE) on the proliferation of human airway epithelial cells and the possible mechanism was studied. After airway epithelial cells were treated with different concentrations of CSE for 24 h, the cell proliferation was measured by MTT and the distribution of different cell cycles by flow cytometry. The FAK expression level was detected by Western blot and the degree of tyrosine phosphorylation by immunoprecipitation. The results showed that CSE could inhibit the proliferation of human airway epithelial cells, arrest the epithelial cells in G1 phase of cell cycle, dramatically decrease the number of epithelial cells in S and G2 phases; Meanwhile CSE could decrease the expression level of FAK and the degree of its tyrosine phosphorylation. The above effects of CSE were concentration-dependent. The expression of FAK and the degree of its phosphorylation was positively correlated to the increased number of epithelial cells in G1 phase, and negatively to the number of epithelial cells in S and G2 phases. It was concluded that the mechanism by which CSE could inhibit the proliferation of human epithelial cells was contributed to the increased expression and activation of FAK.
Bronchi/*cytology ; Bronchi/metabolism ; Cell Cycle/drug effects ; Cell Proliferation ; Cells, Cultured ; Enzyme Activation ; Epithelial Cells/*cytology ; Epithelial Cells/enzymology ; Focal Adhesion Protein-Tyrosine Kinases/biosynthesis ; Focal Adhesion Protein-Tyrosine Kinases/*metabolism ; Phosphorylation ; Tobacco/adverse effects ; Tobacco Smoke Pollution/*adverse effects

Purpose:To detect the abnormalities of WWOX(WW domain containing oxidoreductase) gene in human lung adenocarcinoma cell line A549. Methods:Deletion of WWOX exons 6-8 transcript was analyzed by reverse transcriptase-PCR technology; loss of heterozygosity (LOH) of WWOX gene was analyzed by PCR-based assays for dinucleotide repeat polymorphisms technology. Aberrant expression of WWOX protein was analyzed by western blot. Results:A549 cells samples showed loss of WWOX exons 6-8 transcript.This deletion was not detected in normal primary cultured human bronchial epithelial cells samples.Three microsatellites(D16S3029、D16S3096、D16S504)did not have LOH in the normal primary cultured human bronchial epithelial cells samples, but D16S2029 and D16S3096 were all found to have LOH in A549 Cells samples. We further observed that expression of WWOX protein was significantly lower in A549 cell samples compared to the normal primary cultured human bronchial epithelial cells samples. Conclusions:WWOX gene may be important during tumorigenesis in lung adenocarcinoma cancer.Deletion of exons 6-8,LOH and aberrant expression of protein are all modes of WWOX gene inactivity in lung adenocarcinoma cancer.

AIM: To study the effects of NF-?B decoy oligonucleotides(ODNs) modified with locked nucleic acids(LNA) on gelatinases(MMP-9 and MMP-2) expression and NF-?B activity induced by TNF-? in alveolar macrophages(AM) from patients with chronic obstructive pulmonary disease(COPD).METHODS: AM was collected from bronchoalveolar lavage fluid from patients with COPD.NF-?B decoy ODNs and mismatch ODNs were modified with LNA, and transfected into AM by using Lipofectamine 2000.Then the AM were stimulated for 24 h with TNF-?.Semi-quantitative reverse transcription-polymerase chain reaction(RT-PCR) was used to detect the mRNA expression levels of MMP-9 and MMP-2.MMP-9 protein expression was detected by Western blotting.NF-?B activity was detected by electrophoretic mobility shift assay(EMSA).RESULTS: NF-?B decoy ODNs significantly inhibited MMP-9 and MMP-2 expression induced by TNF-? in AM(P

AIM: To study the effect of BQ123 on voltage-gated K+ current in pulmonary artery smooth muscle cells(PASMCs) from chronic hypoxic rats.METHODS: Twelve age and body weight matched Wistar rats were randomly divided into control and chronic hypoxic group.Single PASMCs were obtained with acute enzyme(collagnaseⅠ plus papain) dispersing method.Using the whole cell patch-clamp technique in freshly isolated PASMCs from normorxic and hypoxic rats,the effects of ET-1 and BQ123,a selective ETA receptor antagonist,on voltage-gated K+ current were recorded.RESULTS:(1) ET-1(10-8 mol?L-1) caused inhibition of K+ current in PASMCs from normoxic and hypoxic rats.The effect of ET-1 on K+ current in PASMCs from hypoxic rats was greater than that from normoxic rats [+50 mV,percent inhibition were(71.04?6.58)% and(60.21?5.32)%,respectively,P0.05,n=5),nor ETA receptor blockade had change of ET-1 mediated IKV inhibition.(3) In chronic hypoxic PASMCs,BQ123 significantly reduced the effect of ET-1 mediated IKV inhibition,from(28.49?6.69) pA/pF to(74.19?9.74) pA/pF at +50 mV(P

AIM: To elucidate whether the mechanism that L-arginine can relieve hypoxia pulmonary hypertension involves inhibition of the activity of protein kinase C(PKC). METHODS: Twenty-one male Wistar rats were randomly divided into NS control, hypoxia and L-arginine(500 mg?kg -1 ?d -1 , ip) treatment groups. After two-weeks treatment, mean pulmonary artery pressure (mPAP), mean systematic artery pressure (mSAP) and the ratio of the weight of right ventricle to that of left ventricle plus septum were measured, then two pulmonary arterial rings were isolated to be exposed to PDBu(a specific activator of PKC ) and observed: (1) The maximal response (P 1) to 500 nmol/L PDBu, the time required to achieve a half-maximal response to 500 nmol/L PDBu (t 1/2 ), the time during which the maximal response to 500 nmol/L PDBu maintained (T) and the isometric responses at different times (2, 4, 8, 12, 20, 40, 60, 80 min). The isometric response was represented as the percentage of the maximal response (P 0) of the same arterial ring to 5?mol/L phenylephrine hydrochloride (P 0%). (2) Dose-response curve in response to PDBu (10-11 000 nmol/L) and the dose producing a half-maximal response in the curve (EC 50 ). RESULTS: mPAP, RV/(LV+S), P 1, T and the isometric responses at 2, 4, 8, 20 min of NS control and L-arginine treatment groups were lower than those of hypoxic group respectively (P

Objective To study the effect of interleukin 13(IL-13)on mucin gene Muc5ac and EGFR expression in mouse lungs. Methods Twenty-four male BALB/c mice were randomly divided into control group and different dose of IL-13 (50ng, 100ng and 250ng) groups, six mice per group. Muc5ac mRNA, and Muc5ac and EGFR protein expressions were detected by RT-PCR and immunohistochemical method, respectively. Results Both Muc5ac and EGFR positive products were located in the cytoplasm of airway epithelial cells. Compared with control group, IL-13 could increase Muc5ac mRNA, and Muc5ac and EGFR protein expressions in dose-dependent manner(all P

Ca~(2+)-activated chloride channels (CaCC, CLCA) are a new family of chloride channels discovered recently, which are related to Ca~(2+)-sensitive chloride ions transport, and there were several members identified currently in different biologic bodies. New studies have shown that its member gob-5 in murine (its human counterpart is CaCC1) plays a pivotal role in airway goblet cell metaplasia, mucus overproduction, MUC5AC gene expression as well as airway hyperresponsiveness (AHR) in asthma, and is a key molecule in the induction of murine asthma and an asthma-related gene. Inhibition of their function and/or their signaling pathway may therefore provide a new therapeutic strategy for asthma.