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1.
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   

2.
AIM: To explore the role of α7 nicotinic acetylcholine receptor (α7nAChR) in anti-inflammation of glucocorticoids (GCs) at physiological concentrations. METHODS: MTT assay was used to measure the viability of BV-2 cells, which were processed by hydrocortisone at different concentrations. On the basis of inflammatory model induced by LPS in BV-2 cells, experimental groups were divided as follows: (1) control; (2) LPS; (3) GCs＋LPS; (4) methyllycaconitine (MLA)＋GCs＋LPS. The levels of TNF-α and IL-1β in the cell supernatants were detected by ELISA. RESULTS: Hydrocortisone at concentrations of 2 000 and 1 000 nmol/L decreased the cell viability to (76.9±5.5)% and (90.8±7.3)%, respectively, indicating the cellular injury by GCs at over-physiological doses. LPS significantly induced the releases of TNF-α and IL-1β in a time- and dose-dependent manner in BV-2 cells. Hydrocortisone at physiological concentrations (500 and 250 nmol/L) reduced the releases of TNF-α and IL-1β in BV-2 cells stimulated by LPS, and MLA at concentration of 10 nmol/L antagonized the anti-inflammatory effect of GCs. CONCLUSION: α7nAChR is involved in the anti-inflammatory effect of the physiological concentrations of GCs.  相似文献   

3.
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   

4.
AIM: To investigate the effects of airway epithelial cells on the phenotype and phagocytosis of macrophages and the roles of hypoxia-inducible factor-1α (HIF-1α).METHODS: Human bronchial epithelial (HBE) cells treated with CoCl2 (0, 100, 200, 400 and 800 μmol/L) or transfected with HIF-1α siRNA were co-cultured with the macrophages differentiated from human monocyte line THP-1 induced by phorbol 12-myristate 13-acetate (PMA). The mRNA expression of HIF-1α in the HBE cells was detected by RT-qPCR. The expression of macrophage surface markers and the phagocytosis rate of E.coli by macrophages were analyzed by flow cytometry.RESULTS: CoCl2 upregulated the mRNA expression of HIF-1α in the HBE cells in a concentration-dependent manner and peaked at 8 h. HBE cells treated with CoCl2 increased the fluorescence intensity ratio of CCL3, CD163, CD206 and CCL18 in co-cultured macrophages, and the strongest effect was seen in the macrophages co-cultured with HBE cells treated with CoCl2 at 800 μmol/L. The fluorescence intensity ratio of CCL3 in co-cultured macrophages increased most obviously at 8 h and 12 h, while the fluorescence intensity ratio of CD163, CD206 and CCL18 increased more prominently in the macrophages co-cultured for 24 h. The stimulating effects of the HBE cells transfected with HIF-1α-Homo-488 siRNA on CCL3, CD163, CD206 and CCL18 in the macrophages were significantly attenuated. The phagocytosis rate of E.coli by macrophages co-cultured with HBE cells treated with different concentrations of CoCl2 for 24 h initially increased (up to 60 min), and then it gradually decreased. Compared with normal HBE co-culture group, the phagocytosis rate in 400 and 800 μmol/L stimulation groups decreased at each time point, and that in 800 μmol/L stimulation group was the most.CONCLUSION: In hypoxia environment, airway epithe-lial cells initially transform macrophages predominantly to an M1-phenotype. However, the long-term hypoxia-stimulated airway epithelial cells inhibit the phagocytosis of macrophages and convert them to M2 superiority. HIF-1α may be an important mediator in these processes.  相似文献   

5.
AIM: To investigate rat Urotensin-II(rat U-II)-induced vasoconstriction of rat main pulmonary arteries and the role of mitogen-activated protein kinase(MAPK). METHODS: The main pulmonary artery was dissected from the male Sprague-Dawley rats and artery ring width was 3-4 mm. Concentration-response curves were generated to rat U-II(0.03 nmol/L-30 nmol/L).Inhibitor of MAPK, PD 98059(0.1 μmol/L-10 μmol/L) were added into the medium after rat U-II(30 nmol/L)induced vasoconstriction had reached plateau to construct the relaxant concentration-response curves and their EC50 and Emax. RESULTS：Rat U-II was a potent vasoconstrictor of isolated rat main pulmonary arteries [EC50=7.95±0.40, Emax=(14.28±6.34)% of the response to 60 mmol/L KCl]; PD 98059 caused concentration-dependent relaxations of rat U-II precontracted arteries [EC50=5.91±0.45, Emax=(81.39±13.65)%]. CONCLUSION: Rat U-II was a potent vasoconstrictor of rat main pulmonary arteries and this response was mediated through MAPK.  相似文献   

6.
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7.
AIM：To investigate the effect of cholestane-3β, 5α, 6β-triol (Triol) on apoptosis of malignant glioma cells. METHODS：C6 cells and A172 cells were incubated with Triol at different concentrations for different time durations. MTT assay was used to detect the cell viability. Hoechst 3f3342 staining and TUNEL assay were used to analyze the cell apoptosis. The caspase activity was measured. The expression of apoptosis-related proteins, Bcl-2 family members, was determined by Western blotting. RESULTS：Triol decreased the cell viability of C6 and A172 cells in a dose- and time-dependent manner and the IC50 values were (17.8±0.6)μmol/L and (20.6±0.2) μmol/L, respectively. Visible nuclei with apoptotic characteristics, significant increase in TUNEL-positive cells, and the activation of apoptotic execution enzyme caspase-3 indicated that cell apoptosis was induced by Triol in both cell lines. After C6 cells were exposed to Triol for 12 h, 24 h and 48 h, the activity of caspase-8 in extrinsic apoptotic pathway and caspase-9 in intrinsic apoptotic pathway was increased time-dependently. Meanwhile, the levels of anti-apoptotic proteins, Bcl-2 and Bcl-xL, was down-regulated, while pro-apoptotic protein Bak was up-regulated in a time-dependent manner. CONCLUSION：Triol induces apoptosis of malignant glioma cells by activating intrinsic and extrinsic apoptotic pathways, and Bcl-2 family members are involved in Triol-induced apoptosis.  相似文献   

8.
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9.
AIM:To investigate the effect of 17β-estradiol on insulin action in cultured C2C12 mytoblasts. METHODS:C2C12 mytoblasts were cultured in 35 mm wells of six-well culture plate in an atmosphere of 5% CO2 at 37℃ in DMEM supplemented with 10% FBS and penicillin/streptomycin(1×105 U/L) to reach 80% confluence. Insulin-resistance C2C12 mytoblasts were obtained by incubating the cells for 24 hours in the presence of a high concentration (5×10-7 mol/L) of insulin. After treatmented with 17β-estradiol (1 nmol/L and 10 nmol/L, respectively) for 24 hours, C2C12 mytoblasts were performed to measure insulin-stimulated 2-DG uptake and GS, PFK, PK activities. RESULTS:17β-estradiol enhanced the capacity of insulin-stimulited 2-DG uptake, increased the GS, PFK and PK activities and prevented insulin-induced resistance in cultured C2C12 mytoblasts. CONCLUSION:17β-estradiol potentiates insulin action and preventes insulin-induced resistance in cultured C2C12 mytoblasts.  相似文献   

10.
AIM: To study the effect of crystallin βB2 on the aging of lens. METHODS: SD rats were maintained routinely and killed at 6 different ages (1 d, 8 d, 2 weeks, 8 weeks, 8 months and 1.5 years). Water-soluble crystallins were extracted and separated by two-dimensional polyacrylamide gel electrophoresis (IEF/SDS-PAGE). After Comassize blue staining, the crystallin patterns were screened and analyzed. βB2 crystallin and the main chaperone proteins (αA2, αB2) were identified and the relative quantity was measured. RESULTS: (1) The quantity of water-soluble crystalline βB2 increased in close relation to the aging of the rat. (2) αA2, αB2 chaperone proteins increased with the aging of the rat too. (3) The change of the quantity of water-soluble crystalline βB2 was closely related to the changes of αA2 , αB2 chaperone proteins. (4) Degraded and modified crystallins began to appear clearly in the lens after 8 months old. CONCLUSION: Based on our results, we infer that water-soluble crystalline βB2 increases with the aging dof the rat, which is helpful to maintain the structure and transparency of the lens.  相似文献   

11.
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   

12.
AIM: To study the expression of glycine receptor α1 subunit in neonatal rat myocardial cells and to investigate the effect of lipopolysaccharide (LPS), hypoxia/reoxygenation, isoproterenol (ISO) and high concentration of glucose (HG) on the expression of glycine receptor α1 subunit in the neonatal rat myocardial cells. METHODS: Neonatal rat myocardial cells were cultured in vitro. The expression of glycine receptor α1 subunit was detected by Western blotting. The neonatal rat myocardial cells were treated with LPS (20 mg/L), ISO (100μmol/L) or high concentration of glucose (25 mmol/L) for 24 h, or were exposed to hypoxia for 3 h followed by reoxygenation for 3 h. Subsequently, the cell viability was measured by CCK-8 assay, and the expression of glycine receptor α1 subunit was determined by Western blotting. RESULTS: The expression of glycine receptor α1 subunit in the neonatal rat myocardial cells was positively detectable by Western blotting. Compared with control group, no significant difference of the cell viability (P>0.05) in LPS group, ISO group, hypoxia/reoxygenation group and HG group was observed. The expression of glycine receptor α1 subunit was increased (P<0.01) in LPS group, ISO group and hypoxia/reoxygenatio group, but decreased (P<0.01) in HG group. CONCLUSION: Glycine receptor α1 subunit exists in the neonatal rat myocardial cells. A certain concentration of LPS or ISO, or hypoxia/reoxygenation for a certain period upregulate the expression of glycine receptor α1 subunit, but HG downregulates the expression of glycine receptor α1 subunit in cultured neonatal rat myocardial cells.  相似文献   

13.
AIM: To investigate the protective effect of quercetin on angiotensin Ⅱ (AngⅡ)-induced cardiomyocyte hypertrophy and its possible mechanism. METHODS: Cardiomyocyte hypertrophy was induced by AngⅡ (100 nmol/L) in primary neonatal cardiomyocytes and H9c2 cells. The cells were treated with different concentration of quercetin (10 μmol/L, 20 μmol/L and 40 μmol/L) for 48 h and then the cardiomyocyte surface areas were measured by immunofluorescence. Proteasome activity was detected by fluorescent peptide substrate. The phosphorylated levels of GSK-3α/β and Akt in H9c2 cells were determined by Western blot. RESULTS: Compared with control group, the cardiomyocyte surface areas were both increased in primary cultured neonatal cardiomyocytes and H9c2 cells, while the surface areas were significantly decreased by quercetin, especially at concentration of 20 μmol/L compared with Ang Ⅱ group (P<0.05). Compared with control group, the chymotrypsin-like, trypsin-like and caspase-like activities of proteasome were all increased in H9c2 cells (P<0.05). The trypsin-like and caspase-like activities of proteasome were inhibited by 20 μmol/L and 40 μmol/L quercetin, while chymotrypsin-like activity was inhibited only at 20 μmol/L of quercetin compared with Ang Ⅱ group (P<0.05). In addition, phosphorylated levels of GSK-3α-Ser21, GSK-3β-Ser9 and Akt-Ser473 in Ang Ⅱ group were all increased compared with control group, which were obviously inhibited by in 20 μmol/L and 40 μmol/L quercetin (P<0.05). CONCLUSION: Quercetin decreases cardiomyocyte hypertrophy through proteasome inhibition, which may be related to the inhibition of Akt and therefore increasing activation of GSK-3α/β in H9c2 cells.  相似文献   

14.
AIM: To elucidate the effect of caveolin-1 on the down-regulation of LPS-induced monocyte chemotactic protein 1 (MCP-1) by 17β-estradiol (E2) in vascular smooth muscle cells (VSMCs).METHODS: The primary-cultured VSMCs were exposed to E2 at concentrations of 10-9-10-6 mol/L. LPS-induced MCP-1 production was assayed by ELISA. The protein expression of caveolin-1 was determined by Western blotting and was silenced by β-methyl cyclodextrin(β-MCD) or caveolin-1 specific siRNA. RESULTS: LPS significantly enhanced MCP-1 production. E2 at concentrations of 10-9-10-6 mol/L inhibited LPS-induced MCP-1 production. The use of caveolin-1 inhibitor β-MCD or silencing the protein expression of caveolin-1 by specific siRNA largely impaired LPS-enhanced MCP-1 production, while E2 markedly inhibited caveolin-1 expression. CONCLUSION: Inhibition of LPS-induced MCP-1 production by E2 is related to the suppression of caveolin-1.  相似文献   

15.
AIM: To elucidate the effect of ginsenoside Rb1 (Gs-Rb1) on the glucose metabolism to improve the viability of the cardiomyocytes under hypoxia, and whether hypoxia-inducible factor 1α (HIF-1α) and/or AMPKα are involved in the process.METHODS: The neonatal rat cardiomyocytes were cultured, and randomly divided into control group, hypoxia (1% O2, 94% N2 and 5% CO2) group, Gs-Rb1 (200 μmol/L) group, Ara-A (500 μmol/L) group, Gs-Rb1+Ara-A group, YC-1 (5 μmol/L) group, Gs-Rb1+YC-1 group, Ara-A+YC-1 group and Gs-Rb1+YC-1+Ara-A group. After the intervention for 8 h, the cell viability was analyzed by MTT assay. The protein levels of AMPK, HIF-1α and glucose transporter-4 (GLUT-4) were determined by Western blot. The activities of heterophosphatase (HK), phosphofructokinase (PFK) and lactic dehydrogenase (LDH) were measured by ELISA.RESULTS: Gs-Rb1 significantly improved the viability of hypoxic cardiomyocytes, which was significantly inhibited by YC-1 and Ara-A. In addition, YC-1 and Ara-A had a synergistic effect. Gs-Rb1 increased the protein levels of AMPK and HIF-1α in the hypoxic cardiomyocytes, which was significantly inhibited by Ara-A and YC-1. Gs-Rb1 significantly increased the expression of GLUT-4 on the cytomembrane of hypoxic cardiomyocytes, which was significantly inhibited by YC-1 or Ara-A, especially Ara-A+YC-1. Gs-Rb1 significantly increased the activities of HK, PFK and LDH, all those were significantly inhibited by YC-1 or Ara-A. Besides, YC-1 and Ara-A had a synergistic effect.CONCLUSION: Gs-Rb1 improves the viability of hypoxic cardiomyocytes, which may be related to the regulation of glucose uptake and enhancement of glycolysis by synergy of both HIF-1α and AMPK.  相似文献   

16.
AIM: To investigate the effect of macrophage peroxisome proliferator-activated receptor α (PPARα) activation on macrophage inflammation-induced activation and migration of cardiac fibroblasts. METHODS: Mouse bone marrow-derived macrophages were treated with vehicle, PPARα agonist WY14643 (10 μmol/L), angiotensin Ⅱ (Ang II; 1 μmol/L) or Ang II+WY14643 for 24 h, and the supernatants were collected as conditioned medium (CM) to stimulate cardiac fibroblasts for additional 24 h. The mRNA levels of PPARα, interleukin-6 (IL-6), IL-1β and tumor necrosis factor-α (TNF-α) in the macrophages as well as fibrotic markers collagen type Ⅰ alpha 2 chain (Col1a2), collagen alpha 1 chain (Col3a1) and actin alpha 2 (Acta2) in the cardiac fibroblasts were detected by RT-qPCR. The protein levels of IL-6 and IL-1β in the macrophages as well as collagen I, collagen III and α-smooth muscle actin (α-SMA; encoded by Acta2 gene) in the cardiac fibroblasts were determined by Western blot. Wound-healing assay was applied to eva-luate the migration ability of cardiac fibroblasts. RESULTS: Ang II significantly increased the mRNA levels of pro-inflammatory factors, such as IL-6, IL-1α and TNF-α, but decreased the mRNA level of PPARα in the macrophages. Administration of PPARα agonist WY14643 dramatically decreased Ang II-induced mRNA levels of IL-6, IL-1β and TNF-α in the macrophages, and significantly decreased Ang II-induced protein expression of IL-6 and pro-IL-1β in the macrophages. The CM from Ang II-treated macrophages significantly up-regulated the mRNA levels of Col1a2, Col3a1 and Acta2 in the cardiac fibroblasts, which were inhibited by the CM from WY14643-treated macrophages. The same results were observed in the protein levels of collagen I, collagen III and α-SMA in the cardiac fibroblasts. Moreover, the CM from Ang II-treated macrophages significantly promoted cardiac fibroblast migration, whereas the CM from WY14643-treated macrophages markedly inhibited macrophage inflammation-induced cardiac fibroblast migration. CONCLUSION: WY14643-activated PPARα inhibits activation and migration of cardiac fibroblasts by attenuating Ang II-induced macrophage inflammatory response.  相似文献   

17.
AIM: To investigate the effect of Thymosin α1 on the development and matutation of thymocytes. METHODS: The proportion of CD4+CD8+ thymocytes and the expression of smoothened (Smo) of the hedgehog (Hh)-signaling in CD4-CD8-thymocytes were examined to observe the effect of thymosin α1 on thymocyte development and matutation. RESULTS: Flowcytometric analysis showed that thymosin α1 showed activity at a low dose of 30 μg/kg, and 30 μg/kg thymosin α1 accelerated the replenishment and maturation of thymocytes according to the expression of Smo of the Hh-signaling in CD4-CD8-thymocytes, the potent negative regulator of proliferative responses. CONCLUSION: Thymosin α1 can accelerates thymocyte development from CD4-CD8- to CD4+CD8+.  相似文献   

18.
AIM: To investigate the role of ATP-sensitive potassium (KATP) channels in the inhibitory effect of hydrogen sulfide (H2S) on high glucose(HG)-induced inflammation mediated by necroptosis in H9c2 cardiac cells.METHODS: The expression levels of receptor-interacting protein 3 (RIP3; an indicator of necroptosis) and cyclooxyge-nase-2 (COX-2) were determined by Western blot. The levels of interleukin-1β (IL-1β) and tumor necrosis factor-α (TNF-α) were detected by ELISA.RESULTS: After H9c2 cardiac cells were treated with 35 mmol/L glucose (HG) for 24 h, the expression of RIP3 was significantly increased. Pre-treatment of the cells with 100 μmol/L diazoxide (DZ; a KATP channel opener) or 400 μmol/L NaHS (a donor of H2S) for 30 min considerably blocked the up-regulation of RIP3 induced by HG. Moreover, pre-treatment of the cells with 100 μmol/L 5-hydroxydecanoic acid (5-HD; a KATP channel blocker) attenuated the inhibitory effect of NaHS on HG-induced up-regulation of RIP3. On the other hand, co-treatment of the cells with 100 μmol/L necrostatin-1 (a specific inhibitor of necroptosis) or pre-treatment of the cells with 100 μmol/L DZ or 400 μmol/L NaHS attenuated HG-induced inflammatory responses, evidenced by decreases in the expression of COX-2 and secretion levels of IL-1β and TNF-α. However, pre-treatment of the cells with 100 μmol/L 5-HD significantly attenuated the above anti-inflammatory effects of NaHS.CONCLUSION: KATP channels play an important role in the inhibitory effect of H2S on HG-induced inflammation mediated by necroptosis in H9c2 cardiac cells.  相似文献   

19.
AIM: To analyze the Effect 17β-estradiol on activated macrophages and possibility of being a target of screening drugs for endometriosis. METHODS: Using scanning electron microscope, the surface of macrophages was observed. Nitric oxide (NO) in supernatant was determined by Griess's reagent. TNF-α was measured by MTT via L929 cells. Using Fluo-3/AM,[Ca2+]i was measured by laser scanning confocal microscopy (LSCM).RESULTS:(1)Increased size,extension of more microvilli,expression of retraction fibers and elaboration of membrane ruffles were detected in 17β-estradiol treated macrophages.(2)17β-estradiol induced NO release from peritoneal macrophages.(3)The more TNF-αwas made by macrophages under the induction of 1β7-estradiol.(4)In-tracellular Ca2+ elevated 39.8%in peritoneal macrophages after 17β-estradiol(100 nmol/L)treatment. CONCLUSIONS: Macrophages were activated by 17β-estradiol at a certain concentration. Activated macrophages by 17β-estradiol may participate in endometriosis and may be a target of screening drugs for endometriosis.  相似文献   

20.
AIM: To investigate the effect of cobalt chloride (CoCl2) on the apoptosis of neural stem cells (NSCs) and the expression of microRNA-26a (miR-26a) in vitro, and to explore the mechanisms of NSC apoptosis induced by CoCl2. METHODS: NSCs were exposed to CoCl2 at different doses (200~600 μmol/L) for 24 h. The cell viability and apoptosis were measured by CCK-8 assay and TUNEL method. The expression of miR-26a-3p, miR-26a-5p, GSK-3β, caspase-3, Bcl-2 and Bax was examined by real-time PCR. The protein levels of Bcl-2 and Bax were detected by Western blotting. RESULTS: The cell viability was inhibited and the apoptosis of NSCs was increased significantly by CoCl2 in a dose-dependent manner (P<0.05). CoCl2 at concentration of 400 μmol/L for 24 h was used to induce apoptosis and the expression of miR-26a was down-regulated compared with control (P<0.05). Exposure to CoCl2 at concentration of 400 μmol/L up-regulated the expression of GSK-3β, caspase-3 and Bax, down-regulated the expression of Bcl-2 and Bcl-2/Bax (P<0.05). CONCLUSION: CoCl2 at concentration of 400 μmol/L induces the apoptosis of NSCs obviously. CoCl2 may induce the NSC apoptosis by mitochondrial apoptotic pathway. Declining miR-26a may be related to NSC apoptosis.  相似文献   

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