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.

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.

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

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 study the effect of proliferating cell nuclear antigen (PCNA) expression on alveolar macrophages (AM) and Fas/FasL expression on alveolar type Ⅱ epithelial cells induced by lipopolysaccharide (LPS) in smoking rats. METHODS: Immunohistochemistry SABC and immunofluorescence techniques were used to examine PCNA expression on AM and Fas/FasL system expression on alveolar type Ⅱ epithelial cells in smoking rats of different stages induced by LPS. RESULTS: The AM PCNA expression in smoking rats reached the highest level after 3 or 4 months. The AM PCNA expression in every groups stimulated by LPS significantly increased ( P

AIM: To investigate the effect of endogenous and exogenous carbon monoxide on the proliferation of pulmonary artery smooth muscle cells under anoxic condition. METHODS: Primary culture of rat PASMCs were passed every 3 days, the 3-5 passages were used. PASMCs were divided into 5 groups, cultured under normoxia and hypoxia and treated with HO inducer hemin, CO scavenger bovine hemoglobin (Hb) and exogenous carbon monoxide (CO), respectively. After 48 hours incubation under the conditions mentioned above, the following assay were carried out: 1) the MTT colorimetric assay and immunocytochemical staining were used to study the energy metabolism and the expression of proliferating cell nuclear antigen (PCNA) in PASMCs. 2) flow cytometry was used to analyze the cell cycle of PASMCs. RESULTS: In comparison with the control group, the value of MTT colorimetric assay was higher, the immunocytochemical staining of PCNA was stronger and the percentages of PASMCs in S and G 2M phases in the anoxia group were higher ( P

AIM: To study the role of adrenomedullin(AM) in the pathogenesis of hypoxic pulmonary hypertension. METHODS: Rats were exposed to chronic hypoxia for 14 days. After the measurement of the right ventricular systolic pressure (RVSP), the rats were executed. The weight of the right ventricle (RV), the left ventricle(LV) and the ventricular septum(SP) were determined. The ration RV/(LV+SP) was used to express the thickness of RV. In situ hybridization was used for the detection of the expression of AM mRNA in the lung and RV. RESULTS: The RVSP in the hypoxic group was (63.63?3.42) mmHg,which was significantly higher than that in control group [(34.13?3.40) mmHg]. The RV/(LV+SP) in hypoxic group was 0.439?0.039,which was increased obviously when compared with that of control (0.230?0.025). The level of AM mRNA expressed in the RV in the hypoxia group was significantly higher than that in the control group. CONCLUSION: The expression of AM mRNA in RV increased in the hypoxic condition, which suggests that AM may attenuate the inappropriate increase in pulmonary artery pressure.

AIM: To explore the effects of levcromakalim(Lev) on pulmonary arterial endothelial cells (PAEC) and smooth muscle cells (PASMC) exposed to hypoxia and the mechanisms involved. METHODS: The effects of Lev on i, and expression of PKC ?, eNOS, iNOS and PDGF-B mRNA and protein levels were observed. The nitrite (NO- 2) and entothelin-1(ET-1) concentrations in supernatant in cultured PAEC and PASMC were measured. The proliferation and apoptosis of PASMC was also detected. RESULTS: When PASMC were exposed to hypoxia, Lev reduced concentration of ET-1 in cultured cell supernatant, lowed the expression of PKC ?, iNOS and PDGF-B both at mRNA and protein levels, decreased i concentration, increased proliferation and promoted the apoptosis in PASMC. However, in the presence of Lev, the i concentration was not changed in the hypoxic PAEC. The NO- 2 concentration in cultured cell supernant and expression of eNOS at mRNA and protein levels in hypoxic PASMC and PAEC were also unchanged. The downregulated ET-1 activity in PASMC and PAEC and proliferation in PASMC involved in the inhibition of PKC ? signaling pathway. CONCLUSIONS: Lev reduce some disadvatage effect of hypoxia on PASMC and PAEC. The mechanism of Lev action may partly involve in the downregulation of PKC ? signaling functions.