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ABSTRACT: To investigate the expression of thrombospondin-1 (TSP-1) in serum and pulmonary arterioles of rats with hypoxic pulmonary hypertension.
Twenty male Wistar rats were divided into two groups and exposed to air and isobaric hypoxia for 3 weeks respectively. The mean pulmonary artery pressure (mPAP) was measured by right cardiac catheterization. The rates of wall thickness/external diameter (WT%) and wall area/total vascular area (WA%) were calculated. The TSP-1 level in serum was measured by enzyme-linked immunosorbent assay. TSP-1 mRNA expression in lung tissue was evaluated by quantitative PCR.
The pulmonary artery pressure increased in the hypoxia exposed rats. The chronic hypoxia also elicited the thicking of the wall and the narrowing of the lumen of pulmonary arterioles. It led to the increases of pulmonary artery pressure, the index of right ventricular hypertrophy [RV/(LV+S)], WA% and WT% compared to the controls [mPAP:(2.86 +/- 0.39) kPa vs. (1.35 +/- 40.28) kPa; RV/(LV+ S): (43.53 +/- 3.38)% vs. (23.68 +/- 3.48)%; WT%: (35.24 +/- 11.20)% vs. (23.63 +/- 9.74)%; WA%: (55.09 +/- 12.38)% vs. (41.62 +/- 12.83)% respectively, P<0.05]. In hypoxic group, the expression of TSP-1 mRNA in the lung was significantly up-regulated, the expression level of TSP-1 in serum was higher than that in control group (P<0.01). Linear correlation analysis showed that TSP-1 mRNA was positively associated with WT%, WA% and mPAP (r= 0.748, 0.686, 0.942 respectively, P<0.05).
The TSP-1 may play an important role in the pathogenesis process of hypoxic pulmonary vascular remodeling and pulmonary hypertension.
Sichuan da xue xue bao. Yi xue ban = Journal of Sichuan University. Medical science edition 11/2012; 43(6):839-42, 887.
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ABSTRACT: To investigate the effect of hypoxia on the expression and production of fractalkine (FKN) in cultured rat pulmonary artery smooth muscle cells (PASMCs) and pulmonary microvascular endothelial cells (PMVECs).
PASMCs and PMVECs from SD rat were cultured in vitro, and were exposed to hypoxia for 12 h,24 h and 48 h. The expressions of fractalkine mRNA and protein in PASMCs and PMVECs were measured by the methods of in situ hybridization and immunohistochemistry. The fractalkine concentrations in supernatant fluid of cultured PASMCs and PMVECs were measured by enzyme-linked immunosorbent assay.
(1) Compared with the control group, the expression and production of fractalkine in PASMCs did not increase after the treatment of hypoxia for 12 hours (P > 0.05), but increased after being treated with hypoxia for 24 hours (P < 0.05), and became more significant after 48 hours (P < 0.01). (2) Compared with the control group, there were no differences of FKN concentrations in supernatant fluid of PMVECs, FKN mRNA and protein levels in PMVECs after being treated with hypoxia for 12 hours, 24 hours or 48 hours (P > 0.05).
Hypoxia stimulates the synthesis and secretion of fractalkine in cultured rat PASMCs.
Sichuan da xue xue bao. Yi xue ban = Journal of Sichuan University. Medical science edition 09/2012; 43(5):661-5.
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ABSTRACT: To investigate the expression of thrombospondin-1(TSP-1) in the lung of hypoxia-induced pulmonary hypertension rats.
Thirty male Wistar rats were divided into two groups, pulmonary hypertension group and control group. The mice in experimental group were exposed to isobaric hypoxia for 3 weeks, and those in control group were exposed to air. The pulmonary artery pressure was measured by right cardiac catheterization. The expression of TSP-1 and TGF-beta1 in the lungs of rats were measured by immunohistochemical staining. The histological sections of the lungs were examined using a computerized image analyzer.
After the induction of hypoxia for 3 weeks, the rats had pulmonary artery pressure increased with the thickening of the wall and the narrowing of the lumen of pulmonary arterioles. In the experimental group, the mean pulmonary artery pressure (mPAP) was (2.86 +/- 0.39) kPa, the index of right ventricular hypertrophy RV/(LV+S) was (43.53 +/- 3.38)%, the ratio of vascular wall thickness/vascular external diameter (WA%) was (55.09 +/- 12.38)%, and the ratio of vascular wall area/total vascular area (WT%) was (35.24 +/- 11.2)%, which all were significantly increased in comparison with those of control group [mPAP (1.35 +/- 0.28) kPa, RV/(LV+S) (23.68 +/- 3.48)%, WT% (23.63 +/- 9.74)%, WA% (41.62 +/- 12.83)%, respectively. P < 0.05). The positive staining of TSP-1 (1.32 +/- 0.04 vs. 0.96 +/- 0.03) and TGF-beta1 (1.38 +/- 0.05 vs. 1.04 +/- 0.04) in the wall of pulmonary arteriole of the rats exposed to hypoxia were significantly stronger than those of control rats (P < 0.01).
The expression of TSP-1 appears to be increased in hypoxic pulmonary hypertension rats, which may contribute to the pathogenesis of hypoxic pulmonary vascular remodeling.
Sichuan da xue xue bao. Yi xue ban = Journal of Sichuan University. Medical science edition 01/2012; 43(1):19-23.
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ABSTRACT: To investigate the effect of fractalkine on cell proliferation of cultured rat pulmonary artery smooth muscle cells (PASMCs) in vitro.
Rat PASMCs were cultured in vitro, and treated with different concentrations (10(-10), 10(-9), 10(-8) mol/L) of fractalkine for 12 h, 24 h and 48 h. The cell proliferation was quantified by MTT assay. The cell cycle of PASMCs was measured by flow cytometric(FCM) analysis.
MTT assay showed that fractalkine promoted significantly the proliferation of PASMCs, and the effect was concentration-dependent. FCM analysis indicated that fractalkine increased the percentage of S phase and proliferative index (PI). The percentage of S phase and PI of PASMCs were increased after treated with fractalkine for 12 hours, which reached a maximal level at 24 hours.
Fractalkine promotes rat PASMCs proliferation in a concentration-dependent manner.
Zhongguo ying yong sheng li xue za zhi = Zhongguo yingyong shenglixue zazhi = Chinese journal of applied physiology 11/2009; 25(4):445-8.
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ABSTRACT: To explore the expression of intercellular adhesion molecule-1 (ICAM-1) in cultured human alveolar type 2 cells (A549) stimulated by mechanical force in vitro.
Cells were divided into 3 groups: a tensile stress group, a compressive stress group and a control group. The four-point bending system was used to stimulate A549 cells. The cells were stimulated by tensile stress or compressive stress respectively at the same magnitude of 1000 microstrain for 6 h. Sham cells in control group were not subjected to mechanical loading. The protein level and mRNA level of ICAM-1 were measured by Western blot and RT-PCR. Then an inhibitor was added to further explore the possible mechanism. The cells were divided into a tensile stress+inhibitor group, a compressive stress + inhibitor group and a control group. The cells were pretreated with PD98059, a specific inhibitor of extracellular signal-regulated kinase (ERK) for 60 min, and then stimulated respectively by tensile stress or compressive stress at the same magnitude of 1000 microstrain for 6 h or were not subjected to mechanical loading. ICAM-1 protein and mRNA concentrations were determined by Western blot and RT-PCR, respectively. The data were analyzed by one-way ANOVA and Student-Newman-Keuls were used to compare 2 means.
The expression of ICAM-1 protein in the tensile stress group (1.16+/-0.07) or the compressive stress group (1.05+/-0.02) were significantly higher than that of the control group (0.78+/-0.07, F=3.31, P<0.05), and the expression of ICAM-1 mRNA in the tensile stress group (1.42+/-0.05) or the compressive stress group (1.27+/-0.05) were also significantly higher than that of the control group (0.13+/-0.04, F=23.1, P<0.01). After pretreated with PD98059 for 60 min, the expression of ICAM-1 protein in the tensile stress group (1.62+/-0.10) was significantly higher than that of the control group (0.50+/-0.03, q=3.75, P<0.05), while there was no significant difference between the compressive stress group (0.60+/-0.03, q=0.32, P>0.05) and the control group. At the transcription level, the expression of ICAM-1 in the tensile stress group (1.57+/-0.03) was significantly higher than that of the control group (0.35+/-0.29, q=3.51, P<0.05), while there was no significant difference between the compressive stress group (0.46+/-0.03, q=0.32, P>0.05) and the control group.
Mechanical forces upregulate the expression of ICAM-1 in A549 cells. PD98059 partly inhibits the upregulation of ICAM-1 induced by mechanical forces. ERK pathway may be partly involved in signal transduction of mechanical force induced expression of ICAM-1 in A549 cells.
Zhonghua jie he he hu xi za zhi = Zhonghua jiehe he huxi zazhi = Chinese journal of tuberculosis and respiratory diseases 03/2009; 32(2):99-102.
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ABSTRACT: CXCR3, via binding its specific ligand CXCL10, plays an important role in cigarette smoke (CS)-induced pulmonary inflammation. CXCR3 is preferentially expressed in activated T cells (chiefly CD8+ T cells). The purpose of this study was to investigate the role of CXCR3 in CS-induced pulmonary injury using CXCR3 gene-deficient (CXCR3-/-) mice.
Differences in the infiltration of inflammatory cells and CD8+ T cells and the expression of inflammatory mediators and chemokines in the bronchoalveolar lavage fluid and lungs at the mRNA and protein levels were compared between CXCR3-/- mice and wild-type (WT) mice at 2 h after 3 d of CS exposure.
Compared with their WT counterparts, the CXCR3-/- mice showed alleviated inflammation, as evidenced by fewer inflammatory cells, particularly cytotoxic CD8+ T cells, in bronchoalveolar lavage fluid and lung tissues. At both the mRNA and protein levels, there were significantly lower levels of inflammatory and chemotactic cytokines, including TNF-alpha, interleukin-8, interferon-gamma, transforming growth factor-beta1, and CXCL10 in the CXCR3-/- mice.
Our data show that CXCR3 is important in recruiting inflammatory cells (particularly CD8+ T cells) into the airways and lungs, as well as initiating inflammatory and fibrotic cytokines release at 2 h following a short-term CS insult. CXCR3 could be a novel target for the treatment of pulmonary inflammation induced by CS.
Acta Pharmacologica Sinica 01/2009; 29(12):1432-9. · 1.95 Impact Factor
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ABSTRACT: To observe the effect of breviscapine on the pulmonary artery pressure and the Rho-kinase and Rho-kinase mRNA in pulmonary arterioles of rats treated with hypoxia, and therefore to explore the mechanisms of breviscapine on hypoxic pulmonary hypertension.
Eighteen adult male SD rats were randomly divided into 3 groups. One group was exposed to air (normal group), the second group was exposed to isobaric hypoxia for 3 weeks (hypoxic group), and the third group was exposed to hypoxia for 3 weeks and treated with breviscapine (preventive group). Cardiac catheterization was used to measure the mean pulmonary arterial pressure (mPAP). The heart was isolated, and the right ventricle (RV), left ventricle plus ventricular septum (LV + S) were weighed to calculate the ratio RV/(LV + S). The ratio of vascular wall thickness/vascular external diameter (WT%) and the ratio of vascular wall area/total vascular area (WA%) were measured by image analysis. The quantity of Rho-kinase and Rho-kinase mRNA in rat pulmonary arterioles were determined by immunohistochemistry and in situ hybridization respectively.
The mPAP in the preventive group [(19.83 +/- 1.47) mm Hg, 1 mm Hg = 0.133 kPa] was significantly lower than that of the hypoxic group [(27.3 +/- 5.0) mm Hg], t = 4.28, P < 0.05. The RV/(LV + S) in the preventive group (0.29 +/- 0.03) was significantly lower than that in the hypoxic group (0.34 +/- 0.05, t = 2.39, P < 0.05). The WT% and WA% in the preventive group (25 +/- 5 and 45 +/- 5, respectively) were significantly lower than those in the hypoxic group (36 +/- 12 and 59 +/- 13, respectively, t = 4.89, 5.89, P < 0.05). The positive staining of ROCKI and ROCKII on pulmonary arterioles in the preventive group (1.18 +/- 0.10 and 1.30 +/- 0.12, respectively) were significantly lower than those in the hypoxic group (1.29 +/- 0.08 and 1.63 +/- 0.24, respectively, t = 3.90, 5.82, P < 0.05). The positive staining of ROCKI mRNA and ROCKII mRNA in the preventive group (1.23 +/- 0.13 and 1.22 +/- 0.06, respectively) were significantly lower than those in the hypoxic group (1.37 +/- 0.13 and 1.59 +/- 0.31, respectively, t = 3.94, 5.83, P < 0.05).
Breviscapine was shown to prevent hypoxic pulmonary hypertension and decrease Rho-kinase and Rho-kinase mRNA.
Zhonghua jie he he hu xi za zhi = Zhonghua jiehe he huxi zazhi = Chinese journal of tuberculosis and respiratory diseases 11/2008; 31(11):826-30.
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ABSTRACT: To investigate the prophylactic effect of thymosin alpha 1 and its mechanism on patients with chronic obstructive pulmonary disease.
Eighty patients with chronic obstructive pulmonary disease were divided into two groups. In the treatment group, 42 patients received thymosin alpha 1 1.6 mg hypodermic injection, quague die alterna, for 10 times. All patients were followed for 6 months, and were assessed the number and days of patients with acute exacerbation at 3 and 6 months. In two groups, before treatment and 3 and 6 months after treatment, the pulmonary function tests were measured, and the blood samples were collected for the measurement of the blood IgA, IgG, IgM, CD3, CD4 and CD8 levels.
In the treatment group, the number and days of patients with acute exacerbation were significantly lower in comparison with those of the control group. After treatment of thymosin alpha 1, blood CD4 and CD4/CD8 levels were significantly increased.
Thymosin alpha 1 has a good protection for the acute exacerbation of chronic obstructive pulmonary disease, by incresing body cellular immune activity.
Sichuan da xue xue bao. Yi xue ban = Journal of Sichuan University. Medical science edition 08/2008; 39(4):588-90.
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ABSTRACT: To evaluate the role of fractalkine in the pathogenesis of hypoxic pulmonary hypertension.
Twenty male SD rats were randomly divided into control group and hypoxic group. Rats in hypoxic group were exposed to hypoxia for 3 weeks. Mean pulmonary arterial pressure (mPAP) was measured by a right cardiac catheterization. The thickness of pulmonary arterioles was measured with a computerized image analyzer. The rates of wall thickness/external diameter (WT%) and wall area/total vascular area (WA%) were calculated. The fractalkine level in lung tissue were measured by enzyme-linked immunosorbent assay. Fractalkine mRNA expression in lung were observed by reverse transcriptase-polymerase chain reaction.
The rat mPAP of hypoxic group was higher than that of the control group [(28.7 +/- 3.8) mmHg vs (16.3 +/- 2.1) mmHg, P < 0.01]. The WT% and WA% were increased significantly in hypoxic group than in control group (WT%: (21.28 +/- 4.60)% vs (10.20 +/- 1.56)%, WA%: (67.08 +/- 9.44)% vs (38.11 +/- 42.30)%, P < 0.01, respectively]. In hypoxic group, the expression of fractalkine mRNA in the lung was significantly up-regulated [(0.49 +/- 0.05) vs (0.29 +/- 0.02), P < 0.01], the expression level of fractalkine in lung tissue was higher than that in control group [(7622.6 +/- 938.4) pg/mL vs (4168.5 +/- 403.5) pg/mL, P < 0.01. Linear correlation analyses showed that fractalkine mRNA and protein were positively associated with WA% and WT% (P < 0.05).
The synthesis and release of fractalkine are increase in the lung tissue of chronic hypoxic rats, and fractalkine may play an important role in hypoxic pulmonary hypertension.
Sichuan da xue xue bao. Yi xue ban = Journal of Sichuan University. Medical science edition 03/2008; 39(2):227-30.
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ABSTRACT: To observe the role of simvasatin, a 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitor, in synthesis and excretion of endothelin-1 (ET-1) in endothelial cell cultured hypoxically.
Human umbilical vein endothelial cells were hypoxically cultured and treated with simvastatin by different concentrations (0, 1.0, 2.5, 5.0, 10.0 micromol/L) and different times (12, 24, 48 h). Mevalonate was used to intervent the effect of simvastatin. Reverse transcription-polymerase chain reaction (RT-PCR)and enzyme-linked immunoadsorbent assay (ELISA) were adopted to measure ET-1 mRNA and ET-1 in supernatant fluid of endothelial cell culture.
(1) There were no changes of ET-1 mRNA and ET-1 expression after the hypoxically cultured endothelial cell were incubated with 1 MICROmol/L simvastatin, but ET-1 expression decreased without significant difference compared to control (0 micromol/L simvastatin) when interfered with 2.5 micromol/L simvastatin. The decreases of ET-1 mRNA and ET-1 expression became more obvious when expression were interfered by 5 micromol/Land 10 micromol/L simvastatin (P < 0.01). (2) ET-1 mRNA and ET-1 expression decreased at 12 h after the endothelial cells were incubated with 10 micromol/L simvastatin, which became more fewer at 24 h and reached the minimum expression at 48 h (P < 0.01). (3) The inhibition effect of simvastatin on ET-1 mRNA and ET-1 expression of endothelial cells could be prevented by mevalonate with concentration of 100 micromol/L.
Simvastatin can inhibit ET-1 expression in endothelial cell cultured hypoxically.
Sichuan da xue xue bao. Yi xue ban = Journal of Sichuan University. Medical science edition 01/2008; 39(1):72-5.
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ABSTRACT: To investigate the change of bone morphogenetic protein-2 (BMP-2) in the lung tissues of rats with hypoxic pulmonary hypertension (HPH) and the role of BMP in the apoptosis of endothelial cells exposed to hypoxia.
Twenty male Wistar rats were randomly divided into two groups, the HPH group and the control group, 10 rats in each group. The HPH model was established by placing the rats in an isobaric chamber [O(2) = (10 +/- 0.5)%] for three weeks. The distribution of BMP-2 in pulmonary tissues was observed by using streptavidin peroxidase method (SP), and the morphologic changes of pulmonary arterioles and the integrated optical density (IA) of BMP-2 were determined by image analysis. The effect of Noggin (a blocking agent of BMP) on the apoptosis of hypoxic cultivated human umbilical vein endothelial cells (HUVEC) was assayed by flow cytometers.
Compared to the control group, pulmonary artery hypertension was evident in the hypoxic rats: mPAP was 16.3 +/- 0.5 mm Hg (1 mm Hg = 0.133 kPa) vs (29.5 +/- 0.9) mm Hg, P < 0.01. In the hypoxic rats, the pulmonary arteriolar wall thickened significantly; WT% was (16 +/- 5)% vs (27 +/- 7)%, and WA% was (54 +/- 11)% vs (80 +/- 8)%, both P < 0.01. The distribution of BMP-2 was mainly in the pulmonary arteriolar walls. The IA of BMP-2 significantly increased (6124 +/- 1199 vs 13 463 +/- 5755, P < 0.01), and showed a positive linear relationship to WT% and WA% respectively (WT%: r = 0.744 P < 0.01; WA%: r = 0.693 P < 0.01). Hypoxia induced apoptosis of HUVEC; the apoptosis rate was increased from 6% to 14% and 25% after exposure to hypoxia for 24 h and 48 h respectively. The HUVEC apoptosis rate induced by hypoxia was reduced by Noggin to 11.91% (24 h) and 15.01% (48 h).
Chronic hypoxia induced an increased expression of BMP-2, and a blocking agent of BMP inhibited the apoptosis of endothelial cells induced by hypoxia. It suggests that BMP may play an important role in the pathogenesis of hypoxic pulmonary hypertension.
Zhonghua jie he he hu xi za zhi = Zhonghua jiehe he huxi zazhi = Chinese journal of tuberculosis and respiratory diseases 10/2007; 30(9):662-6.
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ABSTRACT: In order to evaluate the role of fractalkine in the pathogenesis of hypoxic pulmonary hypertension, we observed the change of serum soluble fractalkine and the expression of fractalkine in pulmonary arterioles of rat at different phase of hypoxia-induced pulmonary hypertension development.
The rat model of hypoxic pulmonary hypertension was duplicated by intermittent hypoxia. Mean pulmonary arterial pressure (mPAP) was measured by a right cardiac catheterization. The thickness of pulmonary arterioles was measured with a computerized image analyzer. Serum soluble fractalkine concentrations were measured by enzyme-linked immunosorbent assay. The expressions of fractalkine mRNA and protein in pulmonary arterioles were detected by in situ hybridization and immunohistochemical analysis, respectively.
Compared to control, the mPAP of rats was markedly elevated after hypoxia for 14 days (P < 0.01), but the index of wall thickness of pulmonary arterioles (WT% and WA%) and the index of right ventricular hypertrophy CRV/(LV+S)] increased significantly at 21 days of hypoxia (P < 0.01). In rats exposed to hypoxia for 21 days, the fractalkine mRNA and protein levels in pulmonary arterioles were up-regulated significantly (P < 0.01), and the serum soluble fractalkine concentrations were also elevated (P < 0.01), as compared with control. Linear correlation analysis showed that the fractalkine mRNA level in pulmonary arterioles was associated with WA% (r = 0.749, P < 0.01) and WT% (r = 0.732, P < 0.01), the fractalkine protein level in pulmonary arterioles was also correlated with WA% (r = 0.727, P < 0.01) and WT% (r = 0.683, P < 0.01).
The chronic hypoxia stimulates the synthesis and release of fractalkine. Fractalkine plays an important role in regulating the pulmonary vascular remodeling.
Sichuan da xue xue bao. Yi xue ban = Journal of Sichuan University. Medical science edition 09/2007; 38(5):756-60.
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ABSTRACT: To investigate the effect of Dragon's Blood on the expression of TGF-beta signal transduction molecule TGFbetaR II or Smad4 mRNA in the lung tissue of rats with pulmonary fibrosis, and to evaluate the effect and its mechanism of Dragon's Blood on pulmonary fibrosis.
30 SD rats were randomly divided into three groups: fibrosis model, treatment and normal control groups. In model group and treatment group, the pulmonary fibrous tissues were induced to form with the intratracheal injection of bleomycin (5 mg/kg). In normal control group, saline was given intratracheally. Dragon's Blood was administered intragastricly in treatment group with a dose of 180 mg/kg diluted in 2 mL saline while saline was given intragastricly to other two groups with same volume from day 2 till day 28 after modeling. All rats were sacrificed on the 29th day. The rat lung histopathology was examined with HE staining. In situ hybridization was used to detect the expressions of TGFbetaR II and Smad4 mRNAs in lung tissue, and the expression of collagen fibril I was examined by an immunohistochemical staining.
The inflammation cell counting in treatment group (12913.78 +/- 5640.12) was significant lower than that in model group (22243.60 +/- 5011.55, P < 0.01). The expression of pulmonary TGF/betaR II mRNA in treatment group was significant lower than that in model group (P < 0.01). In the Smad4 mRNA expression of lung tissue, there was no significant difference occurring between treatment group and model group (P > 0.05). The expression of collagen fibril I in the lung tissue of rats in treatment group was significant lower than that in model group (P < 0. 01).
Dragon's Blood can effectively reduce rats' pulmonary fibrosis, of which the mechanisms may be to inhibit the expression of TGFbetaR II mRNA in the lung tissue and thus to have the preventive effect on the excessive deposit of collagen fibril I.
Sichuan da xue xue bao. Yi xue ban = Journal of Sichuan University. Medical science edition 09/2007; 38(5):802-5.
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ABSTRACT: To explore the role of IL-8 in the pathogenesis of chronic obstructive pulmonary disease (COPD) and the effect of glucocorticoid on COPD.
24 health males of Wistar rats were randomly divided into three groups (group A: normal control group, group B: COPD model group, group C: group pretreated with prednisone), of which each got 8 rats for this study project. Rat COPD model was established by exposing rat to cigarette smoke daily for 120 days. The prednisone was, via stomachal injection, given to the rats of group C with a dose of 5 mg/kg on every other day just before rats exposed to cigarette smoke. After COPD model was set up, the bronchoalveolar lavage (BAL) was performed. The total cells and neutrophils in bronchoalveolar lavage fluid (BALF) were counted for examination, and the levels of IL-8 and TNF-alpha in supernatants of BALF and serum were detected by ELISA. The lung tissue section stained by HE was observed in order to study the alternation of morphology, and also measured in terms of mean lining interval (MLI), mean alveolus number (MAN) and percentage of alveolar area in total area (PAA).
MLI and PAA in group B were higher than those in group A (P < 0.01), and decreased after pretreatment with prednisone (P < 0.01), in which however MAN was just on the contrary. The statistic analysis showed that levels of IL-8 [(114.5 +/- 15.7) pg/mL vs (259.4 +/- 20.1) pg/mL, respectively, P < 0.01], TNF-alpha [(80.5 +/- 9.5) pg/mL vs (145.9 +/- 17.3) pg/ mL, P < 0.01], total cell counts [(1.64 +/- 0.12) x 10(8)/L vs (5.76 +/- 0.29) x 10(8)/L, P < 0.01], neutrophil counts [(0.099 +/- 0.065) x 10(8)/L vs (1.26 +/- 0.25) x 10(8)/L P < 0.01], neutrophil proportion [(5.9 +/- 3. 6)% vs (21.8 +/- 3.7)%, P < 0.05] in BALF of group B were higher than those of group A. After pretreatment with prednisone, the above measured values were significant reduction (P < 0.01 or 0.05). The level of IL-8 in serum of group B was higher than that of group A [(45.2 +/- 13.5) pg/mL vs (85.7 +/- 7.0) pg/mL, P < 0.01], but which, after pretreatment, there was reduction but no significance (P > 0.05). The positive correlation was demonstrated among the levels of IL-8, TNF-alpha and counted neutrophils in BALF of group B, but not between the level of IL-8 and TNF-alpha in serum.
There is a close correlation between IL-8 in BALF and airway inflammation with COPD. The IL-8 cooperating with TNF-alpha may be responsible for the persistence and amplification of airway inflammation with COPD. By modulating the expression of IL-8 gene, inhibiting granulocyte chemotaxis and degranulation, the prednisone may relieve airway inflammation, and relieve the lesion of airway resulting from inflammatory cytokines and cells, hence postpone the progress of COPD.
Sichuan da xue xue bao. Yi xue ban = Journal of Sichuan University. Medical science edition 04/2007; 38(2):287-90.
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ABSTRACT: To investigate the diagnosis value of fibro-optic-bronchoscope combined with tumor maker determination to lung cancer.
By fibro-optic bronchoscope (FB) and electrochemiluminescence (ECL) examinations, 98 cases with lung cancer and 88 cases with benign lung disease were studied for calculating the detectable sensitivity and specificity to lung cancer, then further for evaluating the clinical value of FB examination combined with detection of tumor marker in serum/pleural fluid of patients with lung cancer. Results In patients with lung cancer, the serum levels of CEA, CA125 and CYFRA21-1 were (46.34 +/- 18.28) ng/mL, (83.34 +/- 33.26) U/mL and (25.67 +/- 10.32) ng/mL respectively, which were higher than those in patients with benign lung diseases. The serum levels of above three tumor markers in patients with lung cancer all were significantly higher than those in patients with benign lung diseases (P < 0.05). In the 36 specimens of pleural fluid, three tumor markers were higher than those in the corresponding serum samples. The detectable sensitivity of each tumor marker in pleural fluid was higher than that in serum. The sensitivity, specificity and overall accuracy of CEA in lung cancer were 37.5%, 87.5% and 63.6% respectively, of CA125 were 67.7%, 40.9% and 54.9%; of CYFRA21-1 were 56.3%, 81.8% and 68.5%; of FB were 60.4%, 100.0% and 79.4% respectively. The sensitivity, specificity or overall accuracy of fibro-optic bronchoscope combined with tumor marker (TM) examination to diagnosis of lung cancer was 90.6%, 92.0% or 91.3% respectively.
The FB examination is valuable in diagnosing lung cancer, and by combined with TM determination, can further improve the accuracy to diagnosis of lung cancer.
Sichuan da xue xue bao. Yi xue ban = Journal of Sichuan University. Medical science edition 04/2007; 38(2):312-5.
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Chinese medical journal 10/2006; 119(17):1465-8. · 0.86 Impact Factor
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ABSTRACT: To investigate the change of nuclear factor-kappa B (NF-kappaB) expression in the lung tissues from chronic hypoxic rats and the role of NF-kappaB in the pathogenesis of hypoxic pulmonary hypertension.
Twenty male SD rats were randomly divided into two groups: control group and hypoxic group. The animal model of pulmonary hypertension was established by exposing the rats to normabaric hypoxic conditions for three weeks. The mean pulmonary arterial pressure (mPAP) was measured by a right cardiac catheterization. The indices of wall thickness of pulmonary arteriole (WT% and WA%) were measured by a computerized image analyzer. NF-kappaB expression in lung tissues were observed by using immunohistochemistry.
(1) The mPAP of hypoxic rats was (29.1 +/- 4.5) mmHg,and it was (16.8 +/- 2.6) mmHg in normal rats, there was significant difference between two groups (P < 0.001). (2) In hypoxic group, the WT% was (22.36 +/- 2.99)% and WA% was (69.14 +/- 5.38)%; in normal group, WT% was (15.36 +/- 3.08)% and WA% was (46.75 +/- 6.54)%, the differences were significant (P < 0.01). (3) Both normal and hypoxic group, there were positive cells for NF-kappaB nuclear staining in lung tissues of rats. The percentage of positive cells for NF-kappaB nuclear staining in bronchiolar epithelial cells was significantly increased in the hypoxic group [(29.11 +/- 1.12)%] than that in the control group [(12.23 +/- 1.08)%], P < 0.001.
NF-kappaB expression is increased in the lung tissue of rats with chronic hypoxia. It may play a role in the pathogenic process of hypoxic pulmonary hypertension.
Sichuan da xue xue bao. Yi xue ban = Journal of Sichuan University. Medical science edition 07/2006; 37(4):611-3, 628.
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ABSTRACT: To observe the change of urotensin II (U-II) expression in airways of rat asthmatic models, and of patients with asthma, and therefore to investigate the role of U-II in the pathogenesis of asthma and airway remodeling.
Twenty Wistar rats were divided into a control group (10 rats) and an asthmatic group (10 rats). The animal model of asthma was established by ovalbumin intraperitoneal injection and aerosolization. The internal perimeter of bronchi (Pi), bronchial wall area (WA) and the area of bronchial smooth muscle (WAm) were measured by a computerized image analyzer, and the WA/Pi and WAm/Pi were calculated to express airway remodeling. Autopsy lung tissues from 5 patients with asthma and 5 normal human controls died of car accident were collected, stained with hematoxylin and eosin stain, and the streptavidin peroxidase method. The expression level of U-II and the percentage of positive U-II cell in the airways of rats and patients with asthma were measured.
Rats exposed to ovalbumin developed asthma and airway remodeling: the WA/Pi and WAm/Pi [(24.1 +/- 2.4) microm(2)/microm, (5.3 +/- 1.9) microm(2)/microm] were increased, as compared with the normal group [(16.5 +/- 1.7) microm(2)/microm, (3.8 +/- 1.2) microm(2)/microm], the difference being significant (t = 3.892, 3.785, all P < 0.01). The expression level of U-II in asthmatic rats was 2.46 +/- 0.15, while in the control group was 1.26 +/- 0.11, the difference being significant (t = 6.236, P < 0.01). There was a positive correlation between the level of U-II and WAm/Pi (r = 0.712, P < 0.01). The percentage of positive U-II cells in the asthmatic rats was (82 +/- 8)%, while in the control rats was (22 +/- 8)%, the difference being significant (t = 19.102, P < 0.01). The expression level of U-II in patients with asthma was 2.61 +/- 0.19, while in the control group was 1.36 +/- 0.12, the difference being significant (t = 7.374, P < 0.01). The percentage of positive U-II cells in patients with asthma was (75 +/- 9)%, while in the controls was (27 +/- 7)%, the difference being significant (t = 16.236, P < 0.01).
The expression of U-II is increased in airways of rat asthmatic models and of patients with asthma. It may play an important role in the pathogenesis of asthma and airway remodeling.
Zhonghua jie he he hu xi za zhi = Zhonghua jiehe he huxi zazhi = Chinese journal of tuberculosis and respiratory diseases 07/2006; 29(6):381-4.
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ABSTRACT: To evaluate the expression and the role of Rho-kinase (ROCK I and ROCK II )in the development of hypoxic pulmonary hypertension of rat.
Thirty six of adult male SD rats were randomly divided into six groups; one group was exposed to air as normal control, the other five groups were exposed to isobaric hypoxia for 1 day, 3 days, 1 week, 2 weeks and 3 weeks respectively. Microtube method was used to measure the mean pulmonary arterial pressure (mPAP). The right ventricle (RV) and left ventricle plus atrial ventricular septum (LV+S) were isolated and weighed to calculate the value of RV/(LV+S). The amounts of Rho-kinase and Rho-kinase mRNA in rat pulmonary artery were determined by immunohistochemistry, in situ hybridization and image analysis.
The mPAP and RV/(LV+S) values increased with time prolongation of rats exposed to hypoxia (P<0.05). The ratio of arteriole wall thickness/vascular external diameter(WT%) and vascular area/total vascular area(WA%) went forward to a height with exposing rats to hypoxia for a long time; WT% and WA% of hypoxia group rats exposed for 3 weeks were significantly higher than that of control group (P<0.05). All of ROCK I , ROCK II, ROCK I mRNA and ROCK II mRNA in pulmonary arterioles got the enhanced positive signals of immunohistochemistry staining or in situ hybridization with prolonging the time of rats exposed to hypoxia. The hypoxia group for 3 weeks got significantly stronger staining signals of Rho-kinase and Rho-kinase mRNA in pulmonary arterioles than that of control group (P<0.05). The positive staining of ROCK I , ROCK I mRNA, ROCK II or ROCK II mRNA in pulmonary arterioles all positively related with mPAP, WA% and WT% (r=0.404, 0.267 and 0.263; 0.500, 0.263 and 0.260; 0.490, 0.295 and 0.286; 0.579, 0.251 and 0.254) (P<0.05).
Hypoxia led Rho-kinase and Rho-kinase mRNA to have an increased expression. Rho-kinase may play a role in the development of hypoxic pulmonary hypertension by contracting and remodeling pulmonary arterioles.
Sichuan da xue xue bao. Yi xue ban = Journal of Sichuan University. Medical science edition 05/2006; 37(3):395-8.
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ABSTRACT: To evaluate the preventive effects of montelukast on the collagen expression of pulmonary arterioles in chronic hypoxic rats.
Thirty male Wistar rats were randomly divided into three groups: control group, hypoxic group and montelukast preventive group. The animal model of pulmonary hypertension was established by exposing the rats to normabaric hypoxic conditions 8 hours q.d. for 3 weeks. The expression levels of collagen I and III in arterioles were observed by immunohistochemistry.
The positive degree of collagen I in pulmonary arterioles of hypoxic group was higher than that of control group (1.51+/-0.09 vs 1.15+/-0.05, P<0.01), and the positive degree of collagen I in pulmonary arterioles of preventive group (1.19+/-0.06) was lower than that of hypoxic group (P<0.01). The differences of positive degree of collagen III in pulmonary arterioles were not significant among the three groups (P>0.05).
Montelukast can reduce the hypoxia-induced deposition of collagen I in the pulmonary arterioles wall.
Sichuan da xue xue bao. Yi xue ban = Journal of Sichuan University. Medical science edition 03/2005; 36(2):213-6.
