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1.
AIM: To investigate the effect of platelet-derived growth factor (PDGF) on β3 integrin gene expression and the role of β3 integrin on adhesion, migration and proliferation of vascular smooth muscle cells (VSMC) induced by PDGF. METHODS: β3 integxin gene expression was detected by RT-PCr. After β3 integrin extracellular do-main was blocks, VSMC adhesio, migration and proliferation were measured by adhesion assay awound-culture model an [3H]-TSR incorporation respectively.RESULTS: After the interaction between β3 integrin and extracellular matrix was blocked, VSMC proliferation was inhibited in some degree and the rate of [3H]-TdR incorporation into VSMC decreased 39%. The cell adhesion and migration were significantly inhibited when 10 mg/L anti-β3 integrin antibody was added (P＜0.05). When VSMC were treated by PDGF for 6 hours, the expression of β3 integrin gene was 87% higher than that of control. CONCLUSION: PDGF significantly induces expression of β3 integrin gene in VSMC, and the interaction between β3 integrin and ECM protein may play an important role in VSMC adhesion and migration.  相似文献   

2.
AIM: To study the effect of bFGF on cell proliferation, secretion of type I collagen and expression of integrin β1 in human kidney fibroblasts(KFB). METHODS: The KFB was cultured and stimulated by bFGF in vitro. The proliferation and collagen I secreting of KFB, the expression of integrin β1 were measured by MTT, ELISA and flow cytometer, respectively. RESULTS: bFGF(25-50 μg/L) could obviously stimulate the cell proliferation(P< 0.05), promote the secretion of collagen I(P< 0.05) and enhance the expression of integrin β1(P< 0.05) in human kidney fibroblast. CONCLUSION: bFGF could induce renal interstitial fibrosis by promoting cell proliferation, secretion of collagen I and integrin β1 expression of KFB.  相似文献   

3.
AIM: To study the effect of basic fibroblast growth factor(bFGF) to the expression of integrin β1 subunit of endothelial cells. METHOD: The expression of integrin β1 subunit of endothelial cells was determined before and after bFGF treatment with Western Blot and immage analysis method.RESULTS: The mean gray value of immunostain by immage analysis method is 166.11±9.86 in the experimental group and 175.32±5.12 in the control group, suggested that bFGF may upregulate expression of integrin β1 subunits of endothelial cell. CONCLUSION: bFGF may play an important role in angiogenesis by way of inducing the overexpression of endothelial cell integrin β1 subunits.  相似文献   

4.
AIM: To investigate whether transforming growth factor-β1 (TGF-β1) participates in hypoxia-induced bronchial epithelial-mesenchymal transition (EMT) through lysyl oxidase (LOX). METHODS: Sprague-Dawley (SD) rats were exposed to hypoxia to establish the animal model and were treated with LOX inhibitor β-aminopropionitrile (β-APN). Furthermore, primary rat bronchial epithelial cells were cultured in vitro and exposed either to normoxia or to hypoxia. TGF-β1, TGF-β1 receptor inhibitor (SB431542) or β-APN was used in the cell experiments. The content of collagen was measured by colorimetric method. The expression of TGF-β1, LOX, and 2 EMT-related proteins (namely, the epithelial marker E-cadherin and the mesenchymal marker vimentin) were determined by immunohistochemistry and We-stern blot, respectively. RESULTS: The expression of TGF-β1, vimentin and LOX and cross-linking of collagen were enhanced in hypoxia-exposed rat and in hypoxia-exposed bronchial epithelial cells, but the enhancement was impaired by the treatment with β-APN. In contrast, the expression of E-cadherin was reduced in hypoxia-exposed rat, and was reversed by treatment with β-APN. In vitro experiments demonstrated that TGF-β1 and hypoxia led to the morphological phenotype characteristic of EMT in rat bronchial epithelial cells, in which the morphology of rat bronchial epithelial cells was switched from cobble-stone shape in normoxia-exposed group to spindle fibroblast-like morphology in hypoxia-or TGF-β1-exposed group (P<0.01). Additionally, both β-APN and SB431542 partially prevented TGF-β1 and hypoxia induced EMT in rat bronchial epithelial cells. TGF-β1was able to dose-dependently up-regulate LOX expression in rat bronchial epithelial cells, which was blocked by concurrent incubation with SB431542. The up-regulation of TGF-β1, vimentin, LOX and cross-linking of collagen and down-regulation of E-cadherin in hypoxia-exposed rat bronchial epithelial cells was significantly reversed by incubation with SB431542. CONCLUSION: TGF-β1 regulates hypoxia-induced EMT in bronchial epithelial cells via activation of the LOX.  相似文献   

5.
AIM: To investigate the effects of curcumin (Cur) on the expression of High mobility group box 1 protein (HMGB1), interleukin-1β (IL-1β), tumor necrosis factor-α (TNF-α) in amyloid-β (Aβ)-induced primary rat microglial cells. METHODS: Microglia were derived from the cerebral cortices of postnatal rat brains. The cells were identified by immunocytochemistry using mouse anti rat Iba-1 monoclonal antibody. A cell model using primary rat microglial cells incubated with Aβ25-35 as an inflammation model of Alzheimer's disease (AD) was set up. The morphological characters of primary rat microglial cells were observed. The concentration of Aβ25-35 and the treatment concentration of curcumin were selected by CCK-8 assay. Cultured primary rat microglial cells were divided into 5 groups:normal cell group, Aβ25-35 group, Cur group, Aβ25-35+Cur group and Aβ25-35+DMSO group. The expression of HMGB1, NF-κB, and receptor for advanced glycation end products (RAGE) was detected by Western blot. The levels of HMGB1, IL-1β, and TNF-α in the culture supernatant were measured by ELISA. RESULTS: The purity of primary microglias determined by Iba-1 immunofluorescence was more than 95%. The protein levels of HMGB1, RAGE and NF-κB were significantly increased after Aβ25-35 stimulation. After treatment with Cur, the protein levels of HMGB1, RAGE and NF-κB were significantly decreased (P<0.05). The levels of HMGB1, IL-1β and TNF-α in the supernatant were significantly increased after Aβ25-35 stimulation. Cur significantly decreased the level of HMGB1, IL-1β and TNF-α in the supernatant. CONCLUSION: Curcumin significantly inhibits neuroinflammation stimulated by Aβ25-35 in primary rat microglial cells.  相似文献   

6.
AIM: To observe the expression of Akt/GSK-3β/Snail signaling pathway-related molecules in cisplatin-resistant cell line A549/DDP mediated by transforming growth factor-β1 (TGF-β1), and to explore the association of Akt/GSK-3β/Snail signaling pathway with epithelial-mesenchymal transition (EMT). METHODS: The A549/DDP cells were divided into TGF-β1 (+) group, TGF-β1 (-) group and LY294002 group. The morphological changes of A549/DDP cells treated with TGF-β1 were observed under microscope. The protein expression of E-cadherin and N-cadherin was determined by the methods of immumofluorescence and Western blot. The protein levels of Akt, p-Akt, GSK-3β, p-GSK-3βSer9 and Snail were also detected by Western blot. RESULTS: The A549/DDP cells in TGF-β1 (+) group were dispersive, showed a spindle-like shape and developed pseudopodia. This transformation was conformed to classic EMT markers. Compared with TGF-β1 (-) group, the protein expression of E-cadherin in TGF-β1 (+) group was significantly decreased (P<0.05), and N-cadherin was significantly increased (P<0.05). The protein levels of p-Akt, p-GSK-3βSer9 and Snail were also significantly increased (P<0.05). Compared with TGF-β1 (+) group, the protein levels of p-Akt, p-GSK-3βSer9 and Snail were significantly decreased in LY294002 group (P<0.05). No difference of Akt and GSK-3β expression between TGF-β1 (-) group and TGF-β1 (+) group was observed. CONCLUSION: The mechanism of EMT in A549/DDP cells might be related to Akt/GSK-3β/Snail signaling pathway activated by TGF-β1.  相似文献   

7.
AIM:To explore the effects of different β-adrenergic receptors (β-AR) on the left and right ventricular systolic and diastolic functions in rats under acute hypoxic stress. METHODS:The healthy male SD rats were randomly divided into 4 groups (n=7):control group, non-selected β-AR blocker propranolol group, selected β1-AR blocker atenolol group and selected β2-AR blocker ICI 118,551 group, and then the rats were exposed to normoxia (20.9% O2, 79.1% N2) and hypoxia (15.0% O2, 85.0% N2) condition respectively at the altitude of 2 260 m (Xining, China). The heart rate (HR), the left ventricular systolic pressure (LVSP), the right ventricular systolic pressure (RVSP), and the maximum raise/decline rate of left and right ventricular pressure (±dp/dtmax) were monitored, and the arterial blood gas in normoxia and hypoxia condition were compared to explore the effect of β-AR on the left and right ventricular systolic and diastolic functions in acute hypoxic stress rats. RESULTS:Under normoxia condition, the LVSP, ±dp/dtmax of left ventricular were decreased in propranolol group, atenolol group and ICI 118,551 group, the RVSP and ±dp/dtmax of right ventricle were decreased in propranolol group and atenolol group (P<0.05). Under hypoxia condition, the PaO2, LVSP, ±dp/dtmax of left ventricle were decreased in all groups compared with the normoxia group, and the ±dp/dtmax of right ventricle was increased in all groups (P<0.05), also the degree of index change in control group was more obvious than that in propranolol group and atenolol group. CONCLUSION:The activation of β1-AR is an important compensatory regulation for heart function during hypoxic stress. However, the compensatory enhancement of right heart function under acute hypoxia condition which through tonogenic dilation is more significant for maintaining the normal circulating blood flow.  相似文献   

8.
AIM:To investigate the expression of soluble guanylate cyclase protein and its mRNA in rat pulmonary artery after exposure to hypoxia and hypercapnia.METHODS:Male Sprague-Dawley rats were randomly split into 4 group, which were hypoxic hypercapnic (HH 1 week, HH 2 weeks, HH 4 weeks) group and control group, to copy pulmonary hypertensive animal model. The expression of sGCα1 and β1 subunits protein of medial and small pulmonary artery was performed by immunohistochemistry with a polycolonal antibody. In situ hybridization was performed on the rat lung tissue using sGC oligonuclear probe to assay the expression of sGCα1subunit mRNA.RESULTS:The sGCα1 and β1 subunits protein and sGCα1 subunit mRNA were faint staining in the pulmonary small and medium artery in HH1 week, HH 2 weeks and HH 4 weeks groups compared with control group (all P＜0.01).CONCLUSION:sGC subunit mRNA and protein expression in pulmonary small and medium artery were decreased after exposure to hypoxia and hypercapnia, which took part in the development of the pulmonary hypertension.  相似文献   

9.
AIM: To investigate the effect of lysophosphatidic acid (LPA) on the expression of integrin β6 (ITGB6) for determining the role of transforming growth factor β (TGF-β) activation induced by LPA in this process. METHODS: Normal human bronchial epithelial (NHBE) cells were primarily cultured in 6 well plate and stimulated with LPA. The mRNA expression of ITGB6 and the level of cell surface ITGB6 protein were detected by RT-PCR and flow cytometry,respectively. The activity of active TGF-β induced by LPA was measured by the method of transformed mink lung epithelial cells (TMLC) transfected with TGF-β responsive plasminogen activator inhibitor 1(PAI-1) promoter fused with firefly luciferase reporter gene. RESULTS: After stimulated with LPA at concentration of 10 μmol/L for 2 h, the mRNA expression of ITGB6 in epithelial cells was significantly increased in a time-dependent manner. The results of flow cytometry showed that the protein level of ITGB6 on cell surface was obviously increased after treated with LPA at concentration of 10 μmol/L for 4 h. The active TGF-β induced by LPA in epithelial cells was blocked by an αVβ6 blocking antibody. However, αVβ6 blocking antibody failed to inhibit the mRNA expression of ITGB6 induced by LPA. CONCLUSION: LPA induces the mRNA and cell surface protein of ITGB6 in epithelial cells. The up-regulated ITGB6 expression by LPA is independent on LPA-induced TGF-β activation.  相似文献   

10.
AIM: To study the correlation between phasic change of the relative quantity of major crystallins with aging in rats. METHODS: Six groups of SD rats (age 1 d， 8 d，2 weeks，8 weeks，8 months and 1.5 years) were raised routinely. Water soluble crystallins were extracted and separated by two－dimensional polyacrylamide gelelectrophoresis. After comassize blue staining，the crystallins patterns were scanned and analyzed. RESULTS: (1) Out of the eighteen water soluble major rat crystallins tested in each group, seven showed gradual phasic changes in relative quantity of crystallins, but there were no significant changes in total quantity of water soluble crystallins. (2) Phasic changes in these crystallins presented four different patterns: increasing (βB4、αB2、αA2、βA1), decreasing (β7、β8、γ2,3、γ5,6),relatively stable(βA3、βB5), and irregular. (3) The ratio of βB4 /αA2 increased gradually with the rat aging process. CONCLUSION: The gradual phasic changes in relative quantity of crystallins reflect the aging status of rat crystalline.  相似文献   

11.
AIM: To explore the changes in serum TGF β1 in type 2 diabetes mellitus. METHODS: Forty-five cases type 2 diabetes mellitus patients were divided into three groups according to urine albumim excretion rate(UAER): normoalbuminuria(NA)group and microalbuminuria(MA) group and macroalbuminuria group (Overt DN). Serum TGF β1, fasting blood glucose(FBG), HbA1c,BUN,Cr,Ccr,lipidemia were detected in all cases. RESULTS: Serum TGF β1 in NA, MA and ODN groups was higher than that in control. Serum TGF β1 was positive correlation with Cr(r=0.390,P＜0.05), LDL(r=0.503,P＜0.01), HbA1c (r=0.676,P＜0.01), and UARE(r=0.777,P＜0.01). CONCLUSION: Type 2 diabetes mellitus have a higher serum TGF β1 than controls, serum TGF β1 was positive correlation with HbA1c and injury of renal function.  相似文献   

12.
AIM: To investigate the role of α1 and β2 adrenoceptors(α1AR and β2AR) in the proliferation of hypoxic pulmonary artery smooth muscle cells (PASMCs).METHODS: PASMCs were isolated by an explant method from neonatal bovine pulmonary arteries. The cultured PASMCs were exposed to 6.6% O2 for 6 h, 12 h and 24 h. The method of -TdR incorporation was used to measure the proliferation of PASMCs. i was assayed with Fura-2/AM. The mRNA expression of α1AR, β2AR, c-fos and c-myc was determined by Northern blotting. The effects of activation of α1AR and β2AR, and inhibition of α1AR on the above indexes were observed by treating PASMCs with different AR agonists and antagonists under hypoxic condition.RESULTS: Significant increase in TdR incorporation in hypoxic PASMCs with α1AR activation was observed, and marked decrease in that was induced by α1AR inhibition. However, no significant change was found after β2AR activation. i , the mRNA expression of c-fos, c-myc, α1AR and β2AR in PASMCs were increased after hypoxia.CONCLUSION: Hypoxia induces the increase in i and mRNA expression of c-fos and c-myc, leading to the proliferation of PASMCs. The hypoxic proliferation of PASMCs is intervened by α1AR, but not β2AR. The remodeling of pulmonary arteriole and pulmonary hypertension may be involved in the processes of pulmonary arteriole constriction and proliferation induced by hypoxia through up-regulation of α1AR.  相似文献   

13.
AIM: To investigate the role of endoplasmic reticulum (ES) stress in cardiomyocyte apoptosis induced by β1-adrenoceptor autoantibody (β1-AA). METHODS: The rat model of active immunization with the second extracellular loop of β1-adrenoceptor was established, and SA-ELISA was applied to detect the level of β1-AA in serum of actively immunized rats. The apoptosis of cardiomyocytes was detected by TUNEL staining, and the protein expression levels of glucose-regulated protein 78 (GRP78), C/EBP homologous protein (CHOP) and caspase-12 in rat heart tissues were determined by Western blot and immunohistochemistry. After purified β1-AA obtained by affinity chromatography was used to treat H9c2 myocardial cells, the cell viability was measured by CCK-8 assay and the apoptosis was analyzed by flow cytometry with Annexin V-FITC/PI double staining. The H9c2 cells were treated with ER stress inhibitor 4-phenoxybutyric acid (4-PBA) before interfered with β1-AA, and the changes of cell viability and apoptosis were determined by CCK-8 assay and flow cytometry. RESULTS: Compared with vehicle group, the level of β1-AA in the serum of rats was significantly increased after active immunization for 2 weeks and further rised in 8 weeks, and increased apoptosis was observed in cardiomyocytes after active immunization for 2 weeks, lasting till 8 weeks. Compared with vehicle group, the protein expression of GRP78, CHOP and caspase-12 increased after active immunization for 4 weeks and 8 weeks. Continuous reduction of cell viability and increased apoptosis of H9c2 cells were induced by β1-AA. ER stress inhibitor 4-PBA pretreatment in H9c2 cells reversed the increased apoptosis and decreased cell viability induced by β1-AA, indicating that suppression of ER stress effectively reduced cardiomyocyte apoptosis. CONCLUSION: β1-AA induces increased apoptosis in cardiomyocytes by activating ER stress.  相似文献   

14.
AIM:The purpose of this study was to establish a new strategy for constructing the mouse β2m gene targeting vector in order to increase the homologous recombination frequency in contrast with our previous one, which was successfully constructed in the normal way.METHODS:A 4.2 kb 3' arm and a 0.8 kb 5' arm were amplified by PCR from the mouse β2m-pSV2△HXgpt genomic clone. They included the start region and the three exons, which were separated into two parts from exons 2 (the main coding block) for the two arms——5' arm and 3' arm.RESULTS:The two fragments, in reverse orientation to the Neo gene, were cloned into pPNT respectively on either side of Neo. They were identified by PCR, restriction analysis and sequence analysis as well.CONCLUSION:The mouse β2m gene targenting vector has been cloned successfully.  相似文献   

15.
AIM: To investigate whether chrysophanol alleviates amyloid β-protein (Aβ)-induced cognitive dysfunction and the underlying antioxidative mechanism.METHODS:Adult male Wistar rats (230~250 g) were randomly divided into control group, Aβ1-42 group, chrysophanol group, and Aβ1-42+chrysophanol (1, 10 and 100 mg/kg) groups. Aβ1-42 was delivered by intracerebroventricular injection under the guidence of a brain stereotaxic apparatus. Y-maze test, open-field test and Morris water maze test were performed 1 week after Aβ1-42 injection to evaluate the ability of rat spacial learning and memory. Chrysophanol was intraperitoneally injected once daily for 5 consecutive days. After the behavioral tests, the animals were sacrificed immediately by decapitation, and the hippocampus were collected. The malondialdehyde (MDA) content and the activity of superoxide dismutase (SOD), glutathione peroxidase (GSH-Px) and catalase (CAT) in the hippocampus were measured.RESULTS:Multiple (7 consecutive days, once daily) but not single (once a day) chrysophanol treatment at 1, 10 and 100 mg/kg effectively prevented Aβ1-42-induced cognitive function deficits in a dose-dependent manner as shown by Y-maze test and Morris water maze test. Moreover, the Aβ1-42-induced increase in MDA content and decrease in the activity of antioxidant enzymes (SOD, GSH-Px and CAT) in the hippocampus of the rats were also attenuated by multiple chrysophanol treatment.CONCLUSION:Repeated chrysophanol treatment attenuates Aβ1-42-induced cognitive deficits and synaptic plasticity dysfunction, and the mechanisms underlying the neuroprotective effects are likely due to its antioxidant activity.  相似文献   

16.
AIM: To investigate the effect of high mobility group box-1 protein (HMGB1) on the expression of nuclear factor-κB (NF-κB) in BV-2 cells stimulated with amyloid β-protein (Aβ)25-35. METHODS: Cultured BV-2 cells in logarithmic growth phase were divided into 4 groups:normal cell group (without any treatment), model group (treated with Aβ25-35 at 40 μmol/L), RNA interference (RNAi) group (conducted with HMGB1-siRNA followed by Aβ25-35 stimulation) and solvent control group (treated with 0.1% DMSO). After treatment with Aβ25-35 for 24 h, the protein levels of HMGB1 and NF-κB in BV-2 cells were determined by Western blot. RESULTS: Aβ25-35 at 40 μmol/L was used to stimulate BV-2 cells. The GFP fluorescence-tagged HMGB1-siRNA (30 nmol/L) was used to transfect BV-2 cells and its transfection efficiency was about 80%~90%. The results of Western blot showed that the protein level of HMGB1 was significantly decreased after the interference of siRNA fragment (P<0.05). The protein levels of HMGB1 and nucleic NF-κB p65 were dramatically increased in BV-2 cells stimulated with Aβ25-35 (P<0.05). After RNA interference with HMGB1, the expression of HMGB1 and nucleic NF-κB p65 were significantly decreased in BV-2 cells stimulated with Aβ25-35 (P<0.05). CONCLUSION: RNA interference with HMGB1 reduces the expression of nucleic NF-κB in BV-2 cells stimulated with Aβ25-35.  相似文献   

17.
AIM: To investigate the expression of adhesion molecules in hepatocellular carcinoma (HCC), and analyze its clinical significance. METHODS: The expressions of adhesion molecules of tumor tissues of 64 cases and adjacent tissues of 12 cases of HCC were detected with RT-PCR. RESULTS: ①The expression rates of E-cadherin, ICAM-1, CD44, CD44V, α5, β1 were 90.62%, 93.75%, 50.00%, 96.88%, 100%, 100%, respectively, and there was a significant difference between CD44 and other adhesion molecules. ②The expression level of E-cadherin, ICAM-1, CD44, CD44V, α5,β1 in liver cancer tissues were 1.24±0.54, 0.96±0.37, 0.62±0.73, 0.86±0.33, 0.97±0.49, 1.41±0.24, respectively, and there was a significant difference between CD44 and E-cadherin, β1. ③The expression level of E-cadherin and CD44 mRNA declined as HCC stage become higher, and there was a statistical difference in the expression level of CD44 mRNA between Ⅰ-Ⅱ stage and Ⅳ stage. The expression level of ICAM-1, α5, β1 had a trend to rise as HCC stage become higher, and there was a statistical difference in the expression level of ICAM-1 between Ⅰ-Ⅱ stage and Ⅳ stage. ④The expression level of ICAM-1,CD44V, α5, β1 had positive correlation with tumor volume, tumor nodules, tumor metastasis, and had negative correlation with tumor encapsulation. E-cadherin and CD44 had negative correlation with tumor volume, tumor nodules, tumor metastasis, and had positive correlation with tumor encapsulation. All showed no significant correlation with the level of AFP , the degree of cirrhosis and the function of liver. CONCLUSION: There was a significant difference in the expression level of adhesion molecule mRNA in HCC, and their expression had Spearman correlation with each other. The expression level of adhesion molecule mRNA is associated with tumor volume, tumor nodules and tumor metastasis.  相似文献   

18.
AIM:To investigate the effect of tenuigenin(TEN) on hyperphosphorylation of tau protein in neurons of amyloid β-peptide1-40(Aβ1-40) -induced Alzheimer disease(AD) rats. METHODS:Aβ1-40 was injected into hippocampus CA1 region of the rats to establish AD model. TEN at different doses(18.5 mg/kg, 37.0 mg/kg and 74.0 mg/kg) was intragastrically administered. The protein expression of protein kinase A(PKA),protein phosphatase 2A(PP2A), total tau and p-tau(Ser396) in the neurons was observed by the method of immunohistochemistry. The protein content of total tau and p-tau(Ser396), and the expression level of PKA and PP-2A were detected by Western blotting analysis. RESULTS:In Aβ1-40 group, the level of total tau, the phosphorylation of tau protein and the expression of PKA were significantly increased compared with those in sham operation group. Meanwhile, the expression of PP2A in Aβ1-40 group was lower than that in sham operation group. In TEN treatment group, the level of total tau, the phosphorylation of tau protein and the expression of PKA were markedly decreased, and the expression of PP2A was increased as compared with Aβ1-40 group. CONCLUSION:TEN may protect the neurons from the toxic effect of Aβ1-40 and reduce the hyperphosphorylation of tau(Ser396) in the neurons of AD rats by activating the expression of PP2A and inhibiting the expression of PKA.  相似文献   

19.
AIM: To study the changes of serum autoantibodies against β1-adrenergic and M2-muscarinic receptors in obstructive sleep apnea syndrome (OSAS) patients with chronic obstructive pulmonary disease (COPD), that is, overlap syndrome (OS). METHOD: Serum autoantibodies against β1 and M2 receptors in 26 cases with OS, 32 with OSAS, 30 with COPD and 28 normal subjects were determined by using enzyme-linked immunosorbent assay(ELISA). RESULTS: The positive rates and titer of β1 and M2 receptor autoantibodies are significantly increased in OS group (92.2％,57.7% and 1:98, 1:67), compared to OSAS (71.9%, 40.6% and 1:83, 1:30) or COPD group (70.0%, 36.7% and 1:79, 1:28) (P＜0.05), and they are higher in these groups than in the control (25.0%, 14.3% and 1:20, 1:20) (P＜0.01). CONCLUSION: Serum β1-and M2 receptor autoantibodies are significantly increased in the patients with COPD, OSAS or OS, compared to the control, and the highest is in OS.  相似文献   

20.
AIM: To investigate the effects of all-trans-retinoic acid (ATRA) on the proliferation and differentiation of transforming growth factor β1(TGF-β1)-stimulated human embryonic lung fibroblasts (HFL-I).METHODS: The HFL-I cells were cultured in vitro and were pretreated with ATRA for 3 days at the concentrations of 0.1 μmol/L, 1 μmol/L and 10 μmol/L. The proliferation of HFL-1 cells was detected by MTT method. The mRNA expression of α-smooth muscle actin(α-SMA) in HFL-I cells stimulated with TGF-β1 for 0 h, 6 h, 12 h, 24 h, 48 h and 72 h was detected by RT-PCR and the protein expression of α-SMA at the time points of 1,3 and 5 days was detected by Western blotting. The mRNA expression of α-SMA in HFL-I cells pretreated with different concentrations of ATRA for 24 h was detected the by RT-PCR and the protein expression at time point of 3rd day was detected by Western blotting. RESULTS: Different concentration of ATRA inhibited the proliferation of HFL-I in a dose-dependent manner (P<0.05). Both mRNA and protein expression of α-SMA in HFL-I cells pretreated with TGF-β1 was up-regulated (P<0.05). ATRA down-regulated the mRNA and protein expression of α-SMA induced by TGF-β1 in a dose-dependent manner (P<0.05). CONCLUSION: ATRA inhibits the proliferation and TGF-β1-stimulated differentiation in HFL-I cells by down-regulating the mRNA and protein expression of α-SMA.  相似文献   

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