Objective To assess the effect of atorvastatin on the Lipopolysaccharide (LPS)-induced cyclooxygenase-2 (COX-2) expression in cultured human pulmonary epithelial cells (A549). Methods A549 cells were incubated in the medium containing LPS and different concentrations of atorvastatin(0,10,15,20?M/ml, respectively) for 12h. Then the total cellular RNA and proteins from the cells treated with different experimental conditions were extracted for RT-PCR and western blot analysis,respectively. Results In cultured human pulmonary epithelial cells, atorvastatin reduced the expression of COX-2 mRNA and protein induced by LPS in a dose-dependent manner. Conclusion Atorvastatin may down-regulate LPS-induced COX-2 expression in cultured human pulmonary epithelial cells.

Objective　The aim of this paper was to investigate the reliability and validity of the Chronic respiratory disease questionnaire (CRQ) in China. Method　Sixty-eight patients with chronic respiratory disease who were in hospital from January to November, 1999 were surveyed with CRQ. Eighteen patients were investigated repeatly with CRQ in one week to test the reliability; before and the 10th day after treatment, 50 patients were surveyed twice with CRQ and the peakflow of these patients were also detected. The same doctor explained questionnaires and tested peakflow. Results　The correlated analysis of reliability was positive (r=0.732, P<0.01). The correlatied analysis between the difference of twice-questionnaire scores and the difference of twice-peakflow value was also positive (r=0.565, P<0.01).Conclusion　CRQ can be used by the clinical doctors of China.

AIM:To investigate the effects of high-fat diet on the level of intracellular free calcium ([Ca2+]i) and the activity of angiotensinⅠconverting enzyme (ACE) in alveolar macrophages (AMs) of rabbits. The association between asthma and high-fat diet was also observed. METHODS: Twelve male New Zealand rabbits were medially divided into normal diet group and 1.2% high-cholesterol diet group randomly. 8 weeks later, bronchial alveolar lavage was performed in vitro. [Ca2+]i was determined by Fluo-2/am.The activity of ACE was detected with ultraviolet method. RESULTS: The levels of [Ca2+]i in AMs greatly increased (P

Objective:To investigate the demographic characteristics and the causes for pulmonary hypertension (PH) in adult patients.Methods:A total of 2 508 adult patients diagnosed as PH,who came from the Second Xiangya Hospital of Central South University from January 2010 to December 2014,were retrospectively investigated.All subjects underwent the clinical diagnosis,or the echocardiographic diagnosis,or thetraditional hemodynamic criteria by right heart catheterization (RHC).The patient's data including hospital numbers,gender,ages,primary diseases,etc,are collected and analyzed.Results:In this study,the number of patients diagnosed as PH was increased year by year.The median age of 2 508 patients was 47 (18-93) years old,and there were 933 males (37.2％),the ratio of male to female was 1:1.69 (P＜0.05).Female was more common in Class Ⅰ PH (pulmonary arterial hypertension) and Class Ⅱ PH (pulmonary hypertension due to left heart disease)(＞70％),but there were more male patients (74.5％) in Class Ⅲ PH (pulmonary hypertension due to lung diseases and/or hypoxia).In our study,896 cases (35.73％) were the Class Ⅰ PH,1 163 cases was the Class Ⅱ PH (46.37％),411 cases was the Class Ⅲ PH (16.39％),and the Class Ⅳ PH (chronic thromboembolic pulmonary hypertension) and the Class Ⅴ PH (PH with unclear and/ or multifactorial mechanisms) were diagnosed in 32(1.27％) and 6 patients (0.24％),respectively.The diseases with largest number of patients for the top 7 primary PH were rheumatic heart disease (1 090,43.48％),congenital heart disease (692,27.60％),chronic obstructive pulmonary disease (358,14.28％),connective tissue related disease(156,6.22％),valvular heart disease (66,2.63％),idiopathic PH (46,1.83％) and pulmonary embolism (27,1.08％).Conclusion:Adult PH patients' peak incidence age is 41-50 years old.This disease is more common among women,and the Class Ⅰ/Ⅱ PH are common in women while the Class Ⅲ is more common in men.Rheumatic heart disease and congenital heart disease may be the most common cause for pulmonary hypertension in China,and chronic obstructive pulmonary disease is the most common cause for the Class Ⅲ PH,in which the patients are old.

Objective To determine the effect of atorvastatin on the hypercholesterolemia in-duced lesion in the lung. Methods Fifteen male New Zealand rabbits were randomly assigned into a control group (n=5) , a high-cholesterol forage group (n=5) , and an atrovastatin treatment group (n=5). The control group received normal forage, but the high-cholesterol group and atrovastatin treatment group received high-cholesterol forage. From the 9 th week, the atrovastatin treatment group was added atorvastatin, and the experiment stopped at the end of the 14th week. At the beginning of the experiment and at the 8 th, 14 th week, blood cholesterol and body weight were detected. At the 14th week, bronchial alveolar lavage (BAL) was performed in vitro after the rabbits were executed; pathological examinations were determined in the lung tissues by staining with hamatoxylin-eosin. Oil red 0 and the activities of NF-κB in the alveolar macrophages (AMs) were investigated by immuno-cytochemistry. Proliferative cell nuclear antigen in the lung tissues was adopted by immunohistochem-istry, and the concentrations of IL-6 in the serum, BALF and the culture supematants of AMs were measured by ELISA. Pulmonary tissue paraffin section was stained with hamatoxylin-eosin. Results Atorvastatin reduced inflammatory infiltration, AM NF-κB activation, and cell proliferation in the lung, but raised IL-6 level. Conclusion Hypercholesterolemia-induced pulmonary inflammation is attenuated by atorvastatin.

OBJECTIVE: To investigate whether atorvastatin treatment can improve the symptoms of hypoxia-induced pulmonary hypertension in rats by inhibiting RhoA/Rho kinase pathway. METHODS: A total of 32 Westar rats was divided into 4 groups: normoxic controls (Group A), hypoxic controls (Group B), hypoxia plus atorvastatin [10 mg/(kg.d)] group(Group C), and hypoxia plus the vehicle of atorvastatin (Group D). Rats for hypoxia treatment were maintained under the condition of 10% FiO2 6 h/d for 4 weeks. At the end of 4 weeks, rats were anesthetized and the mean pulmonary arterial pressure (mPAP) was measured by right heart catheterization. The ratios of arteriole wall thickness to vascular external diameter (WT%), and vascular area to total vascular area (WA%) were measured by a computerized image analyzer. RhoA and phos-MYPT-1 expression in the pulmonary artery were determined by Western blot. RESULTS: Comparing with Group A, the mPAP [(29.6 ± 1.1)mmHg vs (16.8 ± 0.7)mmHg], RV/(LV+S) [(39.0 ± 0.7)%vs (29.4 ± 0.5)%], WT% [(35.6 ± 2.4)% vs (22.3 ± 1.2)%] and WA% [(56.5 ± 5.1)% vs (36.6 ± 2.3)%] in Group B were all significantly increased (P<0.05). Comparing with Group B, the mPAP [(25.3 ± 3.2)mmHg], RV/(LV+S) [(36.3 ± 2.1)%], WT%[(29.2 ± 3.2)%] and WA% [(48.1 ± 2.7)%] in Group C were significantly decreased. The vehicle of atorvastatin had no such effect. The expression of RhoA and phos-MYPT-1 in the pulmonary artery was increased in Group B, but it was decreased in Group C. CONCLUSION RhoA/Rho kinase pathway plays an important role in the development of hypoxic pulmonary hypertension. Atorvastatin can improve the symptoms of hypoxic pulmonary hypertension by inhibiting RhoA/Rho kinase activity.
Animals ; Anticholesteremic Agents ; pharmacology ; Atorvastatin ; Hemodynamics ; Heptanoic Acids ; pharmacology ; Hypertension, Pulmonary ; enzymology ; etiology ; physiopathology ; Hypoxia ; complications ; Male ; Pulmonary Artery ; enzymology ; Pyrroles ; pharmacology ; Random Allocation ; Rats ; Rats, Wistar ; Signal Transduction ; drug effects ; Ventricular Remodeling ; drug effects ; rho-Associated Kinases ; metabolism ; rhoA GTP-Binding Protein ; metabolism

OBJECTIVE: To determine effects of the RhoA/Rho kinase signaling pathway on patients with pulmonary arterial hypertension related to chronic obstructive pulmonary diseases by testing levels of Rho-associated coiled-coil containing protein kinase 1(ROCK1) in peripheral blood monocytes in healthy subjects, patients with chronic obstructive pulmonary diseases (COPD), and patients with pulmonary arterial hypertension related to COPD. METHODS: Ten healthy subjects (Group A), 10 patients with COPD (Group B), and 10 patients with pulmonary arterial hypertension related to COPD (Group C) were enrolled, all of whom were hospitalized in the Third Hospital of Changsha between Dec. 2010 and Apr. 2011. Twenty milliliters of blood was collected from each subject. The peripheral blood mononuclear cells (PBMC) were separated by Percoll and, monocytes were incubated. Levels of ROCK1 in the three groups were measured by ELISA. The pulmonary function was measured by spirometric tests, and the pulmonary arterial systolic pressure (PASP) was detected by color Doppler echocardiogram. RESULTS: 1)The PASP in Group C was significantly higher than that of Groups A and B(P<0.01). 2) The levels of ROCK1 in monocytes of Group C were higher than those of Groups A and B(P<0.05). The levels of ROCK1 in monocytes of Group B were higher than those of Group A (P<0.05). 3) The levels of ROCK1 in monocytes of the three groups showed a positive correlation with PASP(r=0.661, P<0.05). 4) The levels of ROCK1 in monocytes of the three groups showed a negative correlation with forced expiratory volume at the first second/ forced vital capacity (FEV1%)(r=0.131, P>0.05). CONCLUSION Rho kinase plays a key role in the pathogenesis of pulmonary arterial hypertension. The ROCK1 may be a marker of the severity of pulmonary arterial hypertension related to COPD.
Aged ; Female ; Humans ; Hypertension, Pulmonary ; etiology ; metabolism ; physiopathology ; Leukocytes, Mononuclear ; metabolism ; Male ; Middle Aged ; Pulmonary Disease, Chronic Obstructive ; complications ; Signal Transduction ; physiology ; rho-Associated Kinases ; blood ; metabolism ; rhoA GTP-Binding Protein ; metabolism

Objective: To observe the conditions of the activating areas in the brain evoked by needling Shenmen (HT 7) acupoint. Methods: Twelve healthy young volunteers were needled at Shenmen (HT 7) acupoint with rotating and twisting techniques. Functional magnetic resonance imaging (fMRI) was adopted to detect the brain activating areas, TR/TE/FA=3560 ms/50 ms/90°. After scanning, the images were dealt with SPM2. Results: Needling Shenmen (HT 7) primarily activated BA2 and BA1 of the gyms postcentralis in right-sided frontal lobe, BA47 of left-sided inferior frontal gyms and BA43 of left-sided gyms postcentralis, and also activated BA40 of inferior parietal lobule in right-sided parietal lobe, BA22 of gyrus temporalis superior in left-sided lobus temporalis, and BA40 of right-sided insula; however, the sham acupoints could not activate these nucleus. Conclusion: Needling Shenmen (HT 7) can activate the relevant functional areas in the brain.

OBJECTIVE: To determine the levels of Rho-kinase and CD4+CD25+ regulatory T cells in patients with asthma, and the relationship between Rho-kinase and CD4+CD25+ regulatory T cells. METHODS: We included 16 patients with moderate to severe asthma in the research group and 14 healthy people as the control group. The levels of Rho-kinase in the 2 groups were measured by ELISA. The level of CD4+CD25+ regulatory T cells in the 2 groups was measured by flow cytometry. The pulmonary function was measured by spirometer. RESULTS: The level of Rho-kinase in the research group was higher than that in the healthy controls (P<0.05). The level of CD4+CD25+ regulatory T cells in the healthy controls was higher than that of the research group (P<0.05). There was no correlation between the level of Rho-kinase in the peripheral blood of the 2 groups and forced expiratiory volume at the first second/ forced vital capacity (FEV1%) (r=-0.491, P>0.05). The level of CD4+CD25+ regulatory T cells in the peripheral blood of the 2 groups showed a positive correlation with FEV1% (r=0.380, P=0.038). There was no correlation between the level of Rho-kinase and the level of CD4+CD25+ regulatory T cells in the peripheral blood of the 2 groups (r=-0.438, P>0.05). CONCLUSION Rho-kinase and CD4+CD25+ regulatory T cells may play a key role in the pathogenesis of asthma.
Asthma ; blood ; Case-Control Studies ; Enzyme-Linked Immunosorbent Assay ; Flow Cytometry ; Forced Expiratory Volume ; Humans ; T-Lymphocytes, Regulatory ; cytology ; Vital Capacity ; rho-Associated Kinases ; blood

OBJECTIVE: To determine the effect of atorvastatin on lipopolysaccharide-induced expression of C-reactive protein in cultured A549 cells. METHODS: A549 cells were incubated in DMEM medium containing lipopolysaccharide in the absence or presence of various concentrations of atorvastatin. After the incubation, the medium was collected and the level of C-reactive protein was measured by enzyme-linked immunosorbent assay. The cells were harvested and C-reactive protein mRNA was analyzed by reverse transcription polymerase chain reaction. RESULTS: Incubation with lipopolysaccharide significantly induced a time and dose dependent increase in the mRNA expression and the production of C-reactive protein in A549 cells (P<0.05). Atorvastatin significantly decreased the lipopolysaccharide induced the mRNA expression and the production of C-reactive protein in a dose dependent manner in A549 cells (P<0.05). CONCLUSION Atorvastatin downregulates lipopolysaccharide-induced expression of C-reactive protein in cultured A549 cells, which may be its mechanism of anti-inflammation.
Atorvastatin ; C-Reactive Protein ; genetics ; metabolism ; Cell Line ; Down-Regulation ; drug effects ; Epithelial Cells ; metabolism ; pathology ; Heptanoic Acids ; pharmacology ; Humans ; Lipopolysaccharides ; antagonists & inhibitors ; Lung ; metabolism ; pathology ; Pyrroles ; pharmacology ; RNA, Messenger ; genetics ; metabolism