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1.
AIM: To investigate the effects of recombinant macrophage migration inhibitory factor (rMIF) on the synthesis of collagen type III in fibroblasts.METHODS: The MRC-5 fibroblasts were divided into 2 groups.The cells in treatment group were exposed to rMIF at the concentrations of 25-100 μg/L for 48 h. The cells without rMIF treatment served as control group. Half an hour before challenging with rMIF (100 μg/L), Y27632 (a Rho-kinase inhibitor) was added to the cells in both 2 groups. After challenged for 48 h, total RNA and protein in the cells were extracted. The expression of collagen type III at mRNA and protein levels was analyzed by RT-PCR and Western blotting, respectively.RESULTS: Different concentrations of rMIF significantly increased the expression of collagen type III at mRNA and protein levels in a dose-dependent manner as compared with the control cells (r=0.862 and r=0.914; all P<0.01). These increases were abolished by Y27632 pretreatment(P<0.01).CONCLUSION: rMIF increases the synthesis of collagen type III in MRC-5 cells and Rho-kinase regulates the MIF-induced synthesis of collagen, suggesting that MIF may play important roles in the pathogenesis of airway remodeling.  相似文献   

2.
AIM: To investigate the influence and the mechanism of recombinant macrophage migration-inhibitory factor (rMIF) on fibroblasts. METHODS: Cultured human embryonic lung fibroblasts (MRC-5 cells) were divided into 2 groups: the cells in treatment group were treated with rMIF (25~100 μg/L) for 24 h or 48 h, and the control cells were without rMIF treatment. The mRNA expression of α-SMA was examined by RT-PCR. The protein level of α-SMA induced by rMIF was quantified by Western blotting. Half an hour before 100 μg/L rMIF challenge, Y27632 was added to the cells of 2 groups. After challenged for 48 h, the total RNA and protein were extracted,and the expression of α-SMA at mRNA and protein levels was determined by means of RT-PCR and Western blotting. After challenged by 100 μg/L rMIF for 6 h, 12 h, 24 h and 48 h, the cell total protein was extracted, and the protein level of α-SMA induced by rMIF was quantified by Western blotting. RESULTS: After stimulation for 24 h, rMIF did not increase the α-SMA mRNA synthesis compared with control. After stimulation for 48 h, rMIF significantly increased the expression of α-SMA mRNA and protein in a dose-dependent manner compared with control (r=0.697 and r=0.957, both P<0.01). Y27632 pretreatment prevented the increase (P<0.01). The amount of phosphorylated MYPT1 increased at 6 h (P<0.01), reached the maximum at 12 h (P<0.01), and decreased but still higher than the control at 24 h and 48 h (P<0.01). CONCLUSION: rMIF increases the α-SMA synthesis in MRC-5 cells and Rho-kinase regulates this process, suggesting that MIF may play important roles in the pathogenesis of airway remodeling.  相似文献   

3.
AIM: To investigate the influence and mechanism of recombinant interleukin-13 (rIL-13) on fibroblasts. METHODS: 3T3 fibroblasts were divided into two groups: the treated group was treated with rIL-13 (80 μg/L, 24 h or 48 h) and the control was without rIL-13 treatment. Transmission electron microscope and Hoechst kit were used to observe morphology of 3T3 fibroblasts in both groups. The activity of proliferation in both groups was investigated and compared by MTT means. Western blot was used to analyze the level of collagen type I induced by rIL-13 in fibroblasts. The levels of IL-6 and IL-8 in the culture supernatants were determined by radioimmunoassay. RESULTS: The more ribosomes and mitochondrions, as well as bigger nuclei were found in the treated group. The production of IL-6 and IL-8, and proliferation ratio of fibroblasts treated with rIL-13 for 24 h or 48 h were increased obviously, compared with the control (P<0.01). The expression of collagen type I protein in treated groups was also significantly higher than that in control (P<0.01). CONCLUSION: rIL-13 upregulates the proliferation of fibroblasts. rIL-13 also has an effect on the production of proinflammatory factors and collagen type I. Taken together, these results suggest that IL-13 may play important roles in the pathogenesis of tissue fibrosis.  相似文献   

4.
AIM:To investigate the effects of thrombospondin 1 on transforming growth factor β1 induced rat cardiac fibroblasts (CFs). METHODS: CFs of neonatal Sprague -Dawley (SD) rats were isolated with the method of digestion and differential anchoring velocity. The proliferation and collagen synthesis of rat CFs were observed with MTT and hydroxyproline. The expression of TSP-1mRNA was analyzed by RT-PCR.RESULTS: The dose and time-dependent effects of TGF-β1 were observed. Expression of TSP-1 was increased significantly (P<0.01). Stimulation of CFs with TGF-β1 (20 μg/L, 24 h) significantly increased CFs proliferation and collagen synthesis (P<0.01). TSP-1 antisense oligonucleotide effectively inhibited TGF-β1 induced CFs proliferation and collagen synthesis (P<0.01).CONCLUSION:The proliferation and collagen synthesis of CFs induced by TGF-β1 are inhibited by TSP-1 antisense oligonucleotide, which may exert helpful effect on anti-fibrosis.  相似文献   

5.
AIM：To investigate the suppressive effect of interferon γ (IFN-γ) on fibrosis induced by interleukin 13 (IL-13) in fibroblasts. METHODS：The fibroblasts were divided into IFN-γ (4×105U/L) group, IL-13 (100 μg/L) group, IFN-γ+IL-13 group and blank control group. At 24 h, 48 h and 72 h, the secreted collagen from fibroblasts was measured by hydroxyproline release assay. The mRNA expression of collagen type I α1 (Col1A1) in fibroblasts was examined by RT-PCR. The protein level of collagen type I synthesized in fibroblasts was analyzed by Western blotting. RESULTS：IFN-γ at 4×105U/ L significantly inhibited the proliferation of fibroblasts and down-regulated Col1A1 mRNA and cellular collagen. The mRNA expression of Col1A1 and the protein level of collagen type I in IFN-γ group were lower than those in blank control group at 48 h and 72 h. At 72 h, the mRNA expression of Col1A1 and the protein level of collagen type I in IL-13 group were substantially higher than those in blank control group, those in IFN-γ + IL-13 group were remarkable lower than those in blank control group, and those in IFN-γ group were also lower than those in blank control group. CONCLUSION：IFN-γ inhibits the fibrotic effect of IL-13 in fibroblasts.  相似文献   

6.
AIM: To explore the effect of high tumor necrosis factor α (TNF-α) level and pre-treatment of epigallocathechin-3 gallate (EGCG) on the process of wound healing in dermal fibroblasts. METHODS: Primary dermal fibroblasts were cultured in vitro. The cells were treated with TNF-α at α concentration of 10 μg/L for 24 h or co-treated with EGCG (40 μmol/L). The cell counting assay was used to observe the proliferation. The cell migration was assessed by wound healing assay. Western blotting was used to observe the expression of collagen type I. RESULTS: High TNF-α level significantly inhibited the proliferation and migration of dermal fibroblasts. However, EGCG pre-treatment attenuated the inhibitory effect of TNF-α on the proliferation in a dose-dependent manner. The inhibited cell migration was also improved by EGCG. The expression of collagen type I was down-regulated by TNF-α and recovered by EGCG pre-treatment. CONCLUSION: EGCG abrogates the inhibitory effect of TNF-α on the proliferation and migration of dermal fibroblasts in wound healing. The expression of collagen type I is also improved. The results suggest that EGCG has protective effect on wound healing.  相似文献   

7.
AIM:To investigate the effects of bilberry anthocyanins on matrix metalloproteinase 2 (MMP2) and collagen type I (collagen I) expression in human fetal scleral fibroblasts (HFSF) in vitro and to provide experimental data for the prevention and treatment of myopia by bilberry anthocyanins. METHODS:HFSF were treated with bilberry anthocyanins at different concentrations (0, 10-6, 10-5, 10-4, 10-3, 10-2, 10-1 and 1 g/L). The effects of bilberry anthocyanins on the viability of HFSF for different time (6 h, 8 h, 12 h, 24 h and 48 h) were measured by MTT assay. The cell cycle distribution and apoptosis of HFSF with highest viability (10-1 g/L bilberry anthocyanins for 12 h) were analyzed by flow cytometry. The mRNA expression of MMP2, COL1A1 and COL1A2 in the HFSF was detected by RT-qPCR. The protein expression of MMP2 and collagen I was determined by Western blot. RESULTS:The cell viability was the highest after treatment with bilberry anthocyanins at a concentration of 10-1 g/L for 12 h. Compared with blank control group, 10-1 g/L bilberry anthocyanin group showed increased cell numbers in S and G2 phases (P<0.05), but no significant difference of the apoptotic rate was observed. The mRNA expression of MMP2 was decreased (P<0.05), and that of COL1A1 was increased (P<0.05). No significant difference of COL1A2 expression was seen. The protein expression of MMP2 was decreased (P<0.05), and collagen I protein was increased (P<0.05). CONCLUSION:Bilberry anthocyanins inhibit the expression of MMP2 and increase the expression of collagen I in the HFSF.  相似文献   

8.
AIM: To explore the effects of decorin on procollagen type I (PcI), mRNA expression,collagen type I synthesis and proliferation of synovial type B cells of stiff knee joint synovial membrane. METHODS: Type B cells of synovial membrane were isolated from the stiff knee joint synovial membrane and cultured in vitro. The cells were treated with decorin at concentrations of 0.1 mg/L, 5 mg/L and 10 mg/L. After cultured for 24 h, 48 h and 72 h, the cell proli-feration rates were measured by MTT colorimetric determination. Cell cycle distribution and apoptosis were analyzed by flow cytometry. The mRNA level of Pc I was detected by RT-PCR, while collagen type I was measured by Western blot. RESULTS: The proliferation of synovial type B cells was significantly inhibited, the percentage of synovial type B cells at G1 phase was significantly increased by 5 mg/L and 10 mg/L decorin (P<0.05), and PcⅠmRNA expression and collagen type I synthesis were significantly decreased. The cells with late apoptosis were not found in control group and experimental groups. CONCLUSION: Recombinant human decorin inhibits synovial type B cell proliferation and decreases PcⅠmRNA expression and collagen type I synthesis in synovial type B cells of stiff knee joint synovial membrane in vitro, suggesting that decorin potentially contributes to the therapy of human knee stiffness.  相似文献   

9.
AIM:To investigate the suppressive effects of dehydroepiandrosterone (DHEA) and glucose-6-phosphate dehydrogenase (G6PD) antisense oligodeoxynucleotides on Raji cells. METHODS:Raji cell line was cultured in vitro in the presence of DHEA at different concentrations ranged from 0.05 μmol/L to 500 μmol/L or G6PD antisense oligodeoxynucleotides. The viability and proliferation of the cells pretreated with dehydroepiandrosterone or G6PD antisense oligodeoxynucleotides were evaluated. Meanwhile, intracellular activities and mRNA expression of G6PD were analyzed. RESULTS:DHEA and G6PD antisense oligodeoxynucleotides does not influence the viability of cells in culture. Raji cells treated with DHEA at concentration of 50 μmol/L or 500 μmol/L for 72 h or with 10.0 μmol/L G6PD antisense oligodeoxynucleotides for 48 h had significant lower cell numbers compared with control (P<0.01). Raji cells treated with DHEA at concentration more than 5.0 μmol/L for 72 h had significant decreased G6PD activities (P<0.01) but no change in mRNA expression levels was observed. With 10.0 μmol/L G6PD antisense oligodeoxynucleotides pretreatment for 48 h, the G6PD mRNA expression levels and activities were significantly decreased (P<0.01). CONCLUSION:DHEA or G6PD antisense oligodeoxynucleotides at specific concentration have suppressive effects on G6PD activities and proliferation in Raji cells to a certain extent, but the suppressive mechanisms are different.  相似文献   

10.
AIM:To explore the mechanism of IGFBP2 and IGFBP4 in hepatocytes with injury induced by TNF-α and TGF-β1. METHODS:Human hepatocyte line (HL-7702) was cultured in vitro and treated with TNF-α or TGF-β1 for 24 h. The expression of IGFBP2 and IGFBP4 was detected by immunochemistry staining. The inhibition ratio of hepatocytes was detected by MTT assay. HL-7702 was treated with TNF-α at concentration of 20 μg/L for 48 h, then the apoptosis of hepatocytes was detected by both Annexin-V /PI and TUNEL assay. RESULTS:The expression of IGFBP2 and IGFBP4 in TNF-α or TGF-β1 treated groups was significantly higher than that in control group (P<0.05). The positive staining of IGFBP2 and IGFBP4 in TNF-α (20 μg/L) treated groups or TGF-β1 (4 μg/L) treated groups was the strongest among all groups. A positive correlation was found between IGFBP2 or IGFBP4 and inhibitory ratio of hepatocytes (P<0.05 or P<0.01). Compared with normal control group, the percentage of apoptosis markedly increased in TNF-α (20 μg/L) treated group (P<0.01). CONCLUSION:IGFBP2 and IGFBP4 involved in the injury process in hepatocytes, indicating an important role in injury of hepatocytes induced by TNF-α or TGF-β1.  相似文献   

11.
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   

12.
AIM: To investigate the effect of activation of retinoid X receptor (RXR) on transforming growth factor β1 (TGF-β1) induced collagen synthesis under hypoxic environment in rat cardiac fibroblasts (CFs) and underlying molecular mechanisms. METHODS: CFs were cultured using myocardial tissue with dry method. Hypoxic environment was established for CFs by continuous nitrogen supplement. Type I and type III collagens in supernatants were detected by ELISA. Nuclear and cytoplasmic extractions were prepared using NE-PER nuclear and cytoplasmic extraction reagents. The protein levels of Smad2 and p-Smad2 were determined by Western blot and immunocytochemical staining. RESULTS: Under hypoxic condition, TGF-β1 (0.01~10 μg/L) increased the synthesis of type I and type III collagens in a dose-dependent manner in the CFs. At the concentration of 5 μg/L, the synthesis of collagen I and III was significantly increased as compared with control group (P<0.01). RXR agonist 9-cis-retinoic acid (9-cis-RA; 10-9~10-6mol/L) decreased TGF-β1 (5 μg/L)-induced synthesis of type I and III collagens in a dose-dependent manner in the CFs under hypoxic condition. The synthesis of type I and type III collagens was significantly inhibited by 9-cis-RA (P<0.01). Smad2 inhibitor (20 nmol/L) showed similar inhibitory effect on the synthesis of type I and III collagens induced by TGF-β1 under hypoxic condition. Compared with TGF-β1 intervention group, the cytoplasmic level of p-Smad2 in the CFs was significantly increased in TGF-β1+9-cis-RA group, but the nuclear p-Smad2 level was significantly decreased (P<0.05). CONCLUSION: Retinoid X receptor agonist 9-cis-RA inhibits TGF-β1-induced synthesis of type I and type III collagens in the CFs by repressing p-Smad2 nuclear translocation under hypoxic condition.  相似文献   

13.
AIM: To study the effects of ［8-(diethylamino) octyl-3, 4, 5 -trimethoxybenzoate］ (TMB-8), an intracellular Ca2+ antagonist, on the activation, proliferation and cell-cycle distribution of the mouse T lymphocytes stimulated by concanvalin A (Con A) in vitro. METHODS: After stimulated with Con A, T cells were treated with different concentrations of TMB-8 alone and its combination with cyclosporine A (CsA). The expression of CD69, the early marker of CD3+ T cell activation, was measured by FACS. The proliferation-related index was determined by carboxyl fluorescin diacetate succinmidyl ester (CFDA-SE) flow cytometry. The cell-cycle distribution was analyzed by propidium iodide staining.RESULTS: After 6 h culture, the activation rate of CD69+ T cell in Con A group was (74.88±1.88)%. 10, 20 and 40 μmol/L of TMB-8 inhibited the expression of CD69 (P<0.01), especially in 40 μmol/L (52.55%±1.54%). After 48 h and 72 h culture, the PI of Con A group was 1.24±0.01, 2.05±0.07, respectively. TMB-8 with the concentration up to 5 μmol/L exerted a definite inhibitory effect on the proliferation with a maximal inhibition in 40 μmol/L(P<0.01). In the combination of 10 μmol/L of TMB-8 with 25 μg/L of CsA, an evident synergistic effect was observed (P<0.01). Moreover, the cell-cycle distribution analysis showed that after 48 h culture, the concentration of TMB-8 over 10 μmol/L showed an evident suppression in S phase.CONCLUSION: TMB-8 significantly inhibites the early steps of the Con A-induced T cell activation and proliferation, as well as the progression of T lymphocytes in S phase.  相似文献   

14.
AIM: The purpose of this study is to investigate the mechanisms related to oxidized low-density lipoprotein (ox-LDL) and dendritic cells (DCs) in the process of atherosclerosis.METHODS: Human DCs were prepared from human CD14+ peripheral blood monocytes using rhGM-CSF (100 μg/L) and rhIL-4 (40 μg/L).Cells were incubated with 100 mg/L native or oxidized LDL for 72 h.The formation of foam cells was investigated by electron microscopy and oil red O staining.Phenotypic and immune functional assays were used with FACS, FITC-dextran phagocytosis, allogeneic mixed T lymphocytes reaction and secretion of Th1/Th2 (IL-12/IL-2) cytokines were also conduced.RESULTS: DCs treated with ox-LDL, but not native LDL were induced into foam cells after cultured for 72 h.Compared with native LDL, ox-LDL-treated DCs were less potent in FITC-dextran phagocytosis.ox-LDL promoted allogeneic T cells proliferation.Moreover, ox-LDL upregulated CD80 (72.4± 9.6 vs 89.5±10.1, P<0.01), CD86 (67.2±8.8 vs 80.2±11.6, P<0.01), HLA-DR (80.6±9.8 vs 86.6±10.8, P<0.01) and CD1a (40.2±10.3 vs 60.2±9.3, P<0.01) expressions, increased IL-12 secretion ［(44.3±8.9)ng/L vs (65.1±10.4)ng/L, P<0.05］ in DCs.However, the secretion of IL-2 was decreased ［(43.6±7.8)ng/L vs (10.0±4.5 )ng/L, P<0.01］ significently.CONCLUSION: DCs were induced into foam cells by ingesting ox-LDL with some functional characteristic of mature DC.DCs seem to be a new source of foam cells and play a key role in immunopathogenesis of atherosclerosis.  相似文献   

15.
AIM:To study the effect of integrin α2 on adhesion of SK-N-SH neuroblastoma cells to collagen.METHODS:Adhesion of the SK-N-SH cells to immobilized collagen w as tested with various concentration of Mg2+,Ca2+ and with 10 μg/L anti-α2 monoclonal antibody (mAb) 6F1.A570 was detected as adhesio n cell numbers.RESULTS:Mg2+-dependent adhesion of SK-N-SH cells to type I collagen was increased significantly,with peak adhesion at concentration of 1 mmol/L Mg2+.A570 with or without Mg2+ was 0.59±0.03 and 0.25±0.01 respectively (P<0.01).No effect of Ca2+ was found on SK-N-SH cell adhesion.6F1 (10 mg/L) blocked the adhesion completely.CONCLUSION:Integrin α2 regulates neuroblastoma cells adhesion t o collagen and suggest that it may play a role in tumor cell migration,invasion and metastasis.  相似文献   

16.
AIM: To observe the role of calcium/calmodulin-dependent protein kinase Ⅱ (CaMKⅡ) in the proliferation, released cytokines and expression of collagen Ⅰ and Ⅲ in rat cardiac fibroblasts induced by angiotensin Ⅱ (AngⅡ) or electrical field stimulation (EFS).METHODS: The cultured cardiac fibroblasts were isolated from the neonatal rats of 1-3 days and used in the 3rd passage. The cells were divided into 10 groups: control group, 0.1 μmol/L AngⅡ group, 0.1 μmol/L AngⅡ+0.5 μmol/L KN92 group, 0.1 μmol/L AngⅡ+0.5 μmol/L KN93 group, 0.1 μmol/L AngⅡ+0.5 μmol/L AIP group; 10V 1.0 Hz EFS group, 10 V 1.0 Hz EFS+0.5 μmol/L KN92 group, 10 V 1.0 Hz EFS+0.5 μmol/L KN93 group, 10 V 1.0 Hz EFS+0.5 μmol/L AIP group, 10 V 1.0 Hz EFS+0.1 μmol/L AngⅡ group.MTT was used to detect the proliferation of cardiac fibroblasts. The release of cytokines was measured by ELISA. The mRNA expression of TNF-α, TGF-β1 and collagen Ⅰ, Ⅲ was determined by RT-PCR.RESULTS: CaMKⅡ inhibitors (0.5 μmol/L KN93 or 0.5 μmol/L AIP) prevented the proliferation and the increase in the expression of TGF-β1 and TNF-α in cardiac fibroblasts induced by AngⅡ (0.1 μmol/L) or EFS (10 V 1.0 Hz). CaMKⅡ inhibitors (0.5 μmol/L AIP or 1.0 μmol/L AIP) also prevented the increase in mRNA expression of collagen Ⅰ and Ⅲ induced by 0.1 μmol/L AngⅡ. CONCLUSION: Inhibition of CaMKⅡ prevents the proliferation of cardiac fibroblasts induced by AngⅡ or EFS. The possible mechanism of CaMKⅡ inhibitors may be involved in preventing the mRNA expression and release of cytokines (TGF-β1 and TNF-α), and regulating collagen I and III expression.  相似文献   

17.
AIM:To evaluate the biological roles of TNF-α on the cartilage endplate cells (chondrocytes). METHODS:The chondrocytes were isolated and harvested from the cartilage endplate of New Zealand rabbits and then the biological characteristics of cells were identified by methods such as toluidine blue staining for type Ⅱ collagen. After different concentrations of TNF-α were added to culture medium respectively, the rate of the proliferation of chondrocytes in different time was measured with MTT. The protein expressions of Bax, Bcl-2, Fas and caspase-3 were measured by immunocytochemistry. The changes of the mRNA of aggrecan and type Ⅱ collagen were measured by RT-PCR. RESULTS:The TNF-α at concentration of 50 μg/L and 100 μg/L decreased the rate of the proliferation on chondrocytes. Though TNF-α at concentrations of 10 μg/L and 50 μg/L increased the level of Bax, Fas and caspase-3, only 50 μg/L TNF-α decreased the level of Bcl-2. TNF-α at concentrations of 10 μg/L and 50 μg/L decreased the level of collagen IIa mRNA and only 50 μg/L TNF-α decreased the level of aggrecan. CONCLUSION:TNF-α not only inhibits the proliferation and the matrix synthesis in chondrocytes, but also increases the expression of pro-apoptotic factors in chondrocytes.  相似文献   

18.
AIM: To observe the effect of leptin (LEP) on hypoxia-reoxygenation induced apoptosis in L02 cells.METHODS: In the experiment, L02 cell injury was induced by hypoxic air (95%N2 and 5% CO2). The cultured L02 cells were divided into hypoxic 12 h group (IR group) alone, normal control group and the hypoxic plus leptin (100 μg/L, 200μg/L, 400 μg/L, 800 μg/L and 1 600 μg/L) treatment groups in vitro. Flow cytometry, terminal dUTP nick-end labeling (TUNEL) assay and fluorescent quantitative PCR were used to measure the changes of apoptosis in L02 cells and expression of Fas/FasL mRNA.RESULTS: (1) The percentage of L02 cells apoptosis and positive TUNEL cells significantly increased in IR group compared to control group (P<0.01). When L02 cells were treated with LEP, the percentage of cell apoptosis and positive TUNEL cells were decreased compared to IR group. (2) Compared to control group, the Fas/FasL mRNA expression significantly increased in IR group (P<0.01). When L02 cells were treated with LEP, the Fas/FasL mRNA expression decreased compared to IR group, the effect of LEP at concentration of 400 μg/L was obviously (P<0.05). CONCLUSION: LEP decreases the apoptosis of hypoxic-reoxygenation L02 cells by down-regulation of Fas/FasL mRNA expression in L02 cells.  相似文献   

19.
AIM: To investigate the effect of CKLF1-C19 polypeptide (C19) on differentiation of human lung fibroblast (LFB) into myofibroblast (MFB) induced by TGF-β. METHODS: LFBs were cultured and identified. LFBs were treated with TGF-β (5 μg/L) to establish the cell model of LFB differentiate into MFB. The LFBs were divided into 6 experimental groups including control group, TGF-β group, and TGF-β plus different doses (1, 0.1, 0.01, 0.001 mg/L) C19 groups. The cell morphology, cell proliferation rate, and the expression of α smooth muscle actin (α-SMA) and collagen I were observed. RESULTS: Human primary LFB was successfully cultured and was confirmed by the method of immunofluorescence. TGF-β at 5 μg/L induced proliferation and differentiation of LFB. The mRNA levels of α-SMA and collagen I in TGF-β group were higher than that in control group (P<0.05).The cell proliferation rates, mRNA levels of α-SMA and collagen I, and the protein expression of α-SMA in 0.01 mg/L+TGF-β group and 0.001 mg/L+TGF-β group were markedly lower than those in TGF-β group (P<0.05). CONCLUSION: C19 at 0.01 mg/L and 0.001 mg/L effectively inhibits differentiation of LFB into MFB induced by TGF-β, thus inhibiting the process of airway remodeling and fibrosis to some extent.  相似文献   

20.
JI Yu-hua  ZENG Yao-ying  YU Yu 《园艺学报》2007,23(8):1590-1592
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