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1.
AIM: To investigate the effect of β-elemene on reversing hepatocyte growth factor (HGF)-induced resistance to gefitinib in PC-9 cells, and to explore its possible mechanisms. METHODS: The gefitinib-resistant PC-9 cells induced by HGF were treated with β-elemene or/and gefitinib. The cell activity was measured by MTT assay. The effect of β-elemene on the invasion ability in HGF-induced resistance to gefitinib in PC-9 cells was detected by Transwell migration assay. The protein levels of p-Met, c-Met, p-AKT and AKT in PC-9 cells of each group were determined by Western blot. RESULTS: The results of MTT assay showed that the cell activity of PC-9 cells was significantly inhibited by β-elemene (P<0.05). IC50 of β-elemene for PC-9 cells was 169.31 mg/L. IC50 of gefitinib for PC-9 cells was 0.30 μmol/L. Exogenously adding recombinant HGF induced significantly resistance to gefitinib in PC-9 cells. Moreover, SU11274 (an inhibitor of c-Met) significantly decreased the viability of the cells exposed to HGF and gefitinib (P<0.05). Combined treatment with β-elemene and gefitinib in the presence of HGF (50 μg/L) significantly decreased the viability of PC-9 cells as compared with the PC-9 cells treated with gefitinib alone in the presence of HGF (P<0.05), so did the result of the cell migration. The protein levels of p-Met and p-AKT were significantly up-regulated by HGF, while the protein levels of p-Met and p-AKT were markedly down-regulated in the cells treated with β-elemene and gefitinib compared with gefitinib alone in the presence of HGF. CONCLUSION: β-elemene reverses HGF-induced resistance to gefitinib in lung cancer PC-9 cells, likely due to the inhibition of HGF-induced activation of c-Met and its down streams signaling pathways (P<0.01). 相似文献
2.
AIM:To investigate the effects of shikonin on the migration, invasion and epithelial-mesenchymal transition (EMT) in human non-small-cell lung cancer PC9 cells induced by hepatocyte growth factor (HGF). METHODS:The effect of shikonin on the viability of PC9 cells was measured by MTT assay. The cell migration and invasion abilities were analyzed by wound healing assay and Transwell method, respectively. The protein expression levels of E-cadherin, N-cadherin and vimentin in the PC9 cells were determined by Western blot. RESULTS:The viability of PC9 cells was significantly inhibited by shikonin in a dose-dependent manner (P<0.01), with IC50 at 9.364 μmol/L. HGF significantly promoted the abilities of migration and invasion, and induced EMT in the PC9 cells. Shikonin significantly inhibited HGF-induced migration and invasion in the PC9 cells. The expression of E-cadherin was significantly down-regulated and the expression of N-cadherin and vimentin was significantly up-regulated in the presence of HGF (50 μg/L). However, shikonin reversed HGF-induced EMT, as indicated by up-regulation of E-cadherin and down-regulation of N-cadherin and vimentin (P<0.01). CONCLUSION:Shikonin reverses HGF-induced EMT in lung cancer PC9 cells. 相似文献
3.
AIM:To investigate the effects of luteolin on the invasion and epithelial-mesenchymal transition (EMT) induced by transforming growth factor-β1 (TGF-β1) in lung cancer A549 cells. METHODS:The effect of luteolin at 5, 10, 20, 40, 80 and 160 μmol/L on the viability of A549 cells was measured by MTT assay. The invasion ability was analyzed by Transwell method. The morphological changes of the A549 cells were observed under microscope.The protein expression of E-cadherin and vimentin in the A549 cells were determined by Western blot. RESULTS:The viability of the A549 cells was significantly inhibited by luteolin in a dose-time dependent manner (P<0.05). The IC50 of luteolin for the A549 cells (24 h) was 68.79 μmol/L, while that (48 h) was 47.86 μmol/L. TGF-β1 induced morphological alteration of the A549 cells from epithelial to mesenchymal forms. Luteolin significantly inhibited TGF-β1-induced invasion of the A549 cells (P<0.01). The protein expression of E-cadherin was significantly down-regulated and the protein expression of vimentin was significantly up-regulated in the presence of TGF-β1 at 5 μg/L (P<0.01). However, luteolin reversed TGF-β1-induced EMT, up-regulation of E-cadherin and down-regulation of vimentin (P<0.01). CONCLUSION:Lu-teolin reverses TGF-β1-induced EMT in the lung cancer A549 cells. 相似文献
4.
AIM: To investigate whether quercitrin induces apoptosis of gastric cancer cell line SGC7901 by inhibition of PI3K/AKT signaling pathway. METHODS: The human gastric cancer SGC7901 cells were selected as the research object. The cytotoxicity of quercitrin was detected by MTT assay, and IC50 value of quercitrin was calculated. The SGC7901 cells were divided into control group, quercitrin group (incubated with 200 μmol/L quercitrin), insulin-like growth factor-1 (IGF-1) group (incubated with 100 μg/L IGF-1) and quercitrin+IGF-1 group (incubated with 200 μmol/L quercitrin and 100 μg/L IGF-1). After 48 h, the apoptosis of SGC7901 cells was analyzed by flow cytometry, and the protein levels of cleaved caspase-3, p-AKT (Ser473), AKT, p-PI3K (Tyr508) and PI3K were determined by Western blot. RESULTS: The viability of SGC7901 cells was significantly decreased as the concentration of quercitrin increased, starting at 100 μmol/L (P<0.05). The IC50 value of quercitrin for 48 h was 275.40 μmol/L. After treatment with 200 μmol/L quercitrin for 48 h, the apoptosis rate and the protein level of cleaved caspase-3 in quercitrin group were significantly increased (P<0.05), and the phosphorylated levels of AKT and PI3K were significantly decreased compared with control group (P<0.05). Treatment with quercitrin and IGF-1 inhibited the effect of quercitrin on SGC7901 cells compared with quercitrin group. CONCLUSION: Quercitrin may induce apoptosis of gastric cancer cell line SGC7901 by inhibiting the activation of PI3K/AKT signaling pathway. 相似文献
5.
AIM:To examine the effects of recombinant human hepatocyte growth factor(rhHGF) and native calf HGF(cHGF) on SMMC-7721 human hepatocellular carcinoma(HCC) cell line. METHODS:Human HCC cell line culture, photometric assay, and flow cytometric assay were used in this study .RESULTS:A similar type of dose-dependent cell growth inhibition effect on SMMC-7721 human HCC cells by rhHGF(5-20 μg/L) as well as by cHGF(25-100 mg/L) had been found, with the maximal effect at the highest concentration used. Approximately over 50% of the cells treated with rhHGF(5 μg/L, 10 μg/L, 20 μg/L) accumulated in the quiescent G0/G1 phase of the cell cycle over incubation periods for 3 d. CONCLUSION:The growth of SMMC-7721 human HCC cells was strongly inhibited by both rhHGF and cHGF. This might be because the cells exposed to HGF became arrested in the G0/G1 phase. 相似文献
6.
AIM: To investigate the effect and mechanism of sodium selenite (Na2SeO3) on the proliferation of endometrial cancer cells. METHODS: Endometrial cancer Ishikawa cells and HEC-1A cells were treated with Na2SeO3. The effect of Na2SeO3 on cell proliferation was determined by MTT assay. The effects of Na2SeO3 on cell cycle distribution and apoptosis were tested by flow cytometric analysis. The expression of cyclin A was detected by Western blotting. RESULTS: Na2SeO3 inhibited the proliferation of Ishikawa cells and HEC-1A cells. For Ishikawa cells, IC50 was 3.26 μmol/L, and for HEC-1A cells, IC50 was 4.77 μmol/L. After treated with Na2SeO3, the cells in G0/G1 phase were reduced and the cells in S phase and G2/M phase were increased. Na2SeO3 also increased the percentage of apoptosis cells. The result of Western blotting showed that the expression of cyclin A was increased. CONCLUSION: Na2SeO3 inhibits the proliferation of endometrial cancer Ishikawa cells and HEC-1A cells via up-regulating the expression of cyclin A, arresting cell cycle and inducing apoptosis. 相似文献
7.
LU Ying LIU Xiang-fu LIU Ling-ling LIN Zhe-sheng CHEN Yu-chan FENG Bao-ying ZHANG Xiang-zhong 《园艺学报》2017,33(1):18-25
AIM: To investigate the effects of celecoxib on viability, apoptosis and autophagy in acute myeloid leukemia (AML) cell lines HL-60 and HL-60A. METHODS: The HL-60 cells and HL-60A cells were cultured with various concentrations (0, 20, 40, 60, 80 and 100 μmol/L) of celecoxib. The inhibitory effect of celecoxib on the cell viability was evaluated by MTT assay. Apoptosis was analyzed by Annexin-V/PI staining. Apoptosis-related and autophagy-related proteins were determined by Western blot. RESULTS: IC50 of celecoxib were 49.4 μmol/L, 32.0 μmol/L and 25.1 μmol/L for HL-60 cells treated with celecoxib for 24 h, 48 h and 72 h, respectively. For HL-60A cells, the corresponding IC50 were 69.1 μmol/L, 42.5 μmol/L and 29.6 μmol/L, respectively. The results of flow cytometry analysis showed the proportions of Annexin-Ⅴ+ PI-, Annexin-Ⅴ+ PI+ and Annexin-Ⅴ-PI+ cells were increased in the HL-60 cells, and those of Annexin-Ⅴ+PI- and Annexin-Ⅴ+ PI+ cells were increased in the HL-60A cells treated with celecoxib for 24 h. After treated with celecoxib, the induction of apoptosis was observed, the apoptosis-related proteins cleaved caspase-3 and cleaved PARP were upregulated, the autophagy-related proteins LC3 II and P62 were both increased, and mTOR, p-mTOR, 4-EBP and p-4-EBP were not changed, indicating that celecoxib inhibited autophagy in the AML cells without the mTOR pathway involvement. CONCLUSION: Celecoxib inhibits the viability of HL-60 cells and HL-60A cells in a time-and dose-dependent manner by its effects of inducing apoptosis and necrosis. Celecoxib inhibits mTOR-independent autophagy in AML cells, indicating a possible way of using celecoxib for enhancing the antitumor activity of therapeutic agents to induce cytoprotective autophagy in the AML cells. 相似文献
8.
AIM: To explore the therapeutic effect of adriamycin combined with rapamycin on endometrial cancer cells. METHODS: Two endometrial carcinoma cell lines with different PTEN gene states were chosen: HEC-1A (wild type) and Ishikawa (mutant type). Before adriamycin administration, the cells were pretreated with low concentration of rapamycin for 24 h. The cell viability and 50% inhibitory concentration (IC50) of adriamycin at 24 h were determined by MTT assay. Multiple drug effect/combination index (CI) was used to evaluate the interaction between adriamycin and rapamycin. Apoptotic rate was measured by flow cytometry. The effects of the drugs on phosphorylation of PI3K/Akt and apoptosis protein caspase-3 were detected by Western blotting. RESULTS: Both adriamycin and rapamycin showed obvious growth inhibitory effects on the 2 endometrial cancer cell lines in a time- and dose-dependent manner. After pretreated with rapamycin, IC50 of adriamycin decreased sharply. In Ishikawa cells, it decreased from (21.3±3.8) μmol/L to(11.9±1.2) μmol/L,P<0.05. In HEC-1A cells, it decreased from (14.3±2.8) μmol/L to (8.2±0.9) μmol/L,P<0.05. Combination index value of the 2 drugs was more than 1.15 in the 2 endometrial cancer cell lines, indicating synergistic effects. The combination therapy of adriamycin with rapamycin increased apoptotic rates in the 2 cell lines, and induced the down-regulation of phosphorylated Akt and over-expression of caspase-3 as compared with single drug treatment (P<0.05). CONCLUSION: Adriamycin combined with rapamycin significantly enhances the chemosensitivity of endometrial cancer cells and reduces drug resistance, which will become a new trend for treating endometrial cancer. 相似文献
9.
MENG Fu-hui CHEN Li XU Shi XIAN Ming ZHANG Hui LI Jian-hua DONG Qi YANG Chun-tao 《园艺学报》2015,31(12):2271-2276
AIM: To investigate the ability of a metal complex ammonium tetrathiomolybdate (ATTM) to release H2S and its cytoprotective effect on an oxidative injury model. METHODS: Released H2S was absorbed in a reaction flask from ATTM dissolved in the cell medium. Staining with dichlorodihydrofluorescein diacetate or rhodamine 123 followed by photofluorography was conducted for the observation of reactive oxygen species (ROS) and mitochondrial membrane potential (ΔΨm) levels, respectively. Cell viability and release of lactate dehydrogenase (LDH) from the cells were measured with commercial kits. RESULTS: Similar to another H2S donor GYY4137, ATTM had an ability to release H2S in the cell medium in a dose-dependent manner. Treatment of human skin HaCaT cells with ATTM at concentrations of 25~400 μmol/L didn't significantly alter cell viability. Exposure of the cells to ultraviolet rays or a ROS donor H2O2 increased the intracellular ROS levels. Treatment with 400 μmol/L H2O2 significantly reduced the viability of HaCaT cells (P<0.01). However, before the treatment with H2O2, pretreatment with ATTM at 100 and 200 μmol/L markedly prevented the H2O2-induced cell injury (P<0.01). In addition, the treatment with H2O2 triggered ΔΨm loss (P<0.01) and LDH release from the cells (P<0.01). Prior to suffering from H2O2 injury, the preconditioning with 200 μmol/L ATTM significantly improved ΔΨm levels (P<0.05) and attenuated LDH release from the cells (P<0.01).CONCLUSION: ATTM is capable of releasing H2S and protecting human skin cells against oxidative injury. 相似文献
10.
YUAN Yu-fen WANG Du-juan PAN Yun-bao LIANG Guang XIAO Jian WANG Su-mei YANG Hui-ling 《园艺学报》2011,27(3):504-508
AIM: To study the effect of curcumin analogues B67 on radioresistant nasopharyngeal carcinoma cells (CNE-2R). METHODS: The effects of B67 on the cell viability and proliferation of CNE-2R and the parent cells CNE-2 were detected by MTT assay and colony formation assay, respectively. The changes of cell cycle, apoptosis and mitochondrial membrane potential were determined by flow cytometry. The morphological changes of the cells were observed under fluorescence microscope. Node mice were subcutaneously inoculated with the cells to determine the tumorigenic ability. RESULTS: The IC50 of B67 on the viability of CNE-2R cells after treatment for 24 h, 48 h and 72 h were 3.96,2.59 and 0.89 μmol/L, respectively, and those of CNE-2 cells were 8.84, 3.55 and 1.10 μmol/L,respectively. The IC50 of B67 on the proliferation of CNE-2R cells after treatment for 48 h was 0.55 μmol/L, and that of CNE-2 cells was 0.73 μmol/L. After treated with B67 for 24 h, CNE-2R and CNE-2 cells at G2/M stage increased from 5.32% to 40.01% and from 9.07% to 15.73%,respectively. After treated with B67 for 48 h, the apoptosis of CNE-2R and CNE-2 cells increased from 5.49% to 38.06% and from 4.99% to 35.74%, respectively. The mitochondrial membrane potential in CNE-2R and CNE-2 cells was decreased by 66.76% and 72.09%, respectively. After treated with B67 for 24 h, the tumorigenic rate of CNE-2R cells was 0%, while the rates of CNE-2 cells in low- and high-concentration groups were 100% and 0%, respectively.CONCLUSION: Curcumin analogue B67 exhibits enhanced suppressive activity on radioresistant nasopharyngeal carcinoma cells by inducing G2/M-phase arrest, promoting cell apoptosis and changing mitochondrial membrane potential. 相似文献
11.
AIM: To investigate the protective effect of hypoxic preconditioning on human bone marrow mesenchymal stem cells (hBM-MSCs), and to provide basic experimental support for more effective autologous stem cell transplantation in aged patients. METHODS: The old hBM-MSCs were subjected to hypoxic preconditioning using a hypoxia incubator chamber for 24 h. The cells were divided into young group, old group and old+hypoxia group (with 24 h hypoxic preconditioning). Hydrogen peroxide (H2O2, 300 μmol/L) was applied to simulate the oxidative stress. The cells were treated with 50 μmol/L LY294002 for 2 h to inhibit PI3K/AKT pathway. BrdU incorporation and CCK-8 assay were used for analyzing the cell proliferation and viability. The protein levels of Bax, Bcl-2 and p-AKT were measured by Western blot. RESULTS: BrdU-positive cells, which represented the cell proliferation, and the cell viability were significantly increased in old+hypoxia group compared with old group (P<0.05). The protein level of Bax decreased (P<0.05) and Bcl-2 increased (P<0.05) in old+hypoxia group compared with old group after using 300 μmol/L H2O2 simulate. the oxidative stress. The phosphorylation of AKT was enhanced by hypoxic preconditioning in old group (P<0.05). The protective effect of hypoxic preconditioning on the cell survival was decreased after treated with LY294002 (inhibitor of the PI3K/AKT pathway) (P<0.05). CONCLUSION: Hypoxic preconditioning increases the survival and proliferation of old hBM-MSCs by activation of AKT pathway. 相似文献
12.
AIM: To investigate the effect of glibenclamide (Glib) on the viability and acid-base equilibrium of glioblastoma cells. METHODS: U251 cells and U87 cells were treated with Glib at different concentrations. The inhibitory rates were detected by CCK-8 assay. The effective dose was screened and the experiment was divided into control group and drug treatment groups. The migration ability was monitored by wound healing assay, and intracellular pH was detected by pH indicator fluorescent probe. The protein expression levels of inwardly-rectifying potassium channel 4.1 (Kir4.1) and monocarboxylate transport protein 1 (MCT1) were determined by Western blot. RESULTS: The half maximal inhibitory concentrations (IC50) of Glib for 48 h exposure of U251 cells and U87 cells were 400.20 μmol/L and 553.70 μmol/L, respectively. The effective inhibition doses of Glib for U251 cells were from the ranges of 100 μmol/L to 1 600 μmol/L, and those for U87 cells were from 50 μmol/L to 1 600 μmol/L in a concentration-dependent manner (P<0.05). Glib not only inhibited the migration (P<0.05) of U251 cells and U87 cells, which was negatively correlated with drug concentration (P<0.05), but also reduced the intracellular fluorescence intensity in experimental group (P<0.05), suggesting that with the increase in drug concentration, the intracellular pH decreased gradually (P<0.05). The protein expression of Kir4.1 and MCT1 was down-regulated by treatment with Glib, and was negatively correlated with concentration of Glib. CONCLUSION: Glib, a kind of potassium channel blocker, induces intracellular acidification via down-regulating the expression of Kir4.1 and MCT1, thus inhibiting the growth of glioblastoma in a certain dose range. 相似文献
13.
LIU Guan-yu HE Wei-yang ZHU Xin YANG Fan HUANG Xiao-long YIN Hu-bin GOU Xin 《园艺学报》2015,31(12):2176-2182
AIM: To investigate whether oxidative stress is able to induce autophagy in mesenchymal stem cells (MSCs), and to explore the effects of autophagy on MSC proliferation and apoptosis under oxidative stress circumstance as well as the underlying mechanism for promoting the therapeutic effects of transplanted MSCs on treating diabetes mellitus erectile dysfunction (DMED). METHODS: Hydrogen peroxide (H2O2) was applied to simulate the oxidative stress circumstance. The effects of H2O2 at concentration of 0, 50, 100, 200, 400 μmol/L on the viability of MSCs were tested by the method of Trypan blue exclusion and MTT assay respectively . The methods of MTT assay, Western blot and transmission electron microscope (TEM) were used to explore the effects of H2O2 on MSC apoptosis and autophagy. RESULTS: The proliferation of MSCs was obviously inhibited by H2O2 in a dose-dependent manner (P<0.01) and the 50% inhibiting concentration (IC50) was (384.58±16.89) μmol/L. H2O2 induced apoptosis and autophay of MSCs. The proliferation rate of MSCs was suppressed by H2O2 significantly (P<0.05), with a further decline by blockade of autophagy (P<0.05) whereas increased by blockade of apoptosis (P<0.05). H2O2 induced MSCs apoptosis obviously (P<0.05), with an augment of apoptosis (P<0.05) by blockade of autophagy. Furthermore, the H2O2 increased expression of cleaved caspase-3 and cleavage of poly ADP-ribose polymerase 1 (PARP1), Which were decreased by apoptosis blockade whereas were enhanced by blockade of autopahgy. CONCLUSION: Oxidative stress plays a dual role in MSC survival, which induces MSC apoptosis and autophagy. Moreover, blockade of autophagy intensifies MSC apoptosis. Therefore, it is a promising method to ameliorate the effects of stem-cell based therapy on DMED by enhancing protective autophagy to increase the survival rate of transplanted MSCs against oxidative stress circumstance caused by diabetes mellitus. 相似文献
14.
AIM: To investigate the anticancer effect of manumycin on abdominal metastatic breast cancer cell line - SK-BR-3 and its relationship with p38 MAPK. METHODS: The test of anticancer effect was performed by the method of MTT, apoptosis induced by manumycin and affected by SB203580, a specific p38 MAPK inhibitor, were examined by caspase-3 activity assay kit, and the protein expression was detected by immunoblotting assay. RESULTS: The inhibition rates at 24 h after treatment with manumycin of 6 μmol/L, 18 μmol/L, 54 μmol/L were (7.4±3.9)%, (21.0±4.4)% and (64.7±4.1)%, respectively and showed dosage-effect relationship. Compared with the control group, the survival rates of the last two treatment groups were decreased significantly (P<0.01). The value of IC50 24 h after treatment with manumycin was 42.5 μmol/L. Manumycin simultaneously activated caspase-3 protein, which was partly blocked by p38 MAPK inhibitor, SB203580. The results of immunoblotting showed that manumycin increased p38 MAPK protein phosphorylation. CONCLUSION: Manumycin exerts anticancer effect on SK-BR-3 cell line via inducing cell apoptosis, which is partly regulated by p38 MAPK. 相似文献
15.
AIM: To investigate the effect of hirsutine on hypoxia-induced migration and invasion abilities of human breast cancer MCF-7 cells and its possible mechanism. METHODS: CCK-8 assay was employed to detect the cytotoxic effect of hirsutine on the MCF-7 cells. Cell migration was observed by wound healing assay, and cell invasion ability was measured by Transwell invasion assay. Western blot was used to analyze the protein levels of hypoxia-inducible factor-1α (HIF-1α), Snail, E-cadherin and matrix metalloproteinase-9 (MMP-9). The mRNA levels of HIF-1α was detected by RT-PCR. RESULTS: Hirsutine remarkably reduced the cell viability from 32 μmol/L (P<0.05), and the IC50 value was 62.82 μmol/L. In hypoxia state, MCF-7 cells showed more powerful capabilities of migration and invasion (P<0.05), higher protein levels of HIF-1α, Snail and MMP-9 (P<0.05), lower protein level of E-cadherin (P<0.05), and higher mRNA level of HIF-1α (P<0.05). These hypoxia-induced effects were all inhibited by hirsutine at 16 μmol/L (P<0.05), apart from the mRNA level of HIF-1α. CONCLUSION: Hirsutine inhibits hypoxia-induced migration and invasion in human breast cancer MCF-7 cells most likely via down-regulation of the protein levels of HIF-1α, Snail and MMP-9, and up-regulation of the protein level of E-cadherin. 相似文献
16.
PPARγ mediates effects of diosgenin on proliferation and apoptosis in human glioblastoma U87MG cells
AIM:To investigate the effect of diosgenin (Dio) on the proliferation, apoptosis and expression of peroxisome proliferator-activated receptor γ (PPARγ) in human glioblastoma U87MG cells and its possible mechanism. METHODS:Human astrocytes (HA) and U87MG cells were cultured in vitro and treated with Dio (0, 10, 20, 30, 40 and 50 μmol/L) and GW9662 (5 μmol/L) for 48 h, and then the cell viability was detected by CCK-8 assay. Cell colony formation assay was used to assess the proliferation potential. Flow cytometry was used to analyze the cell cycle distribution and apoptosis. The mRNA expression level of PPARγ was measured by RT-PCR. Western blot was used to determine the protein levels of PPARγ, cyclin D1, cyclin E1, Bcl-2 and Bax. RESULTS:Dio had no significant influence on the viabi-lity of HA (P>0.05). However, Dio remarkably reduced the viability of U87MG cells in a dose-dependent manner (P<0.05) with IC50 of 24.31 μmol/L. Meanwhile, Dio remarkably diminished colony formation ability (P<0.05), induced G0/G1 phase arrest of the cell cycle and apoptosis (P<0.05), up-regulated the expression of PPARγ at mRNA and protein levels, increased the protein level of Bax (P<0.05), and down-regulated the protein levels of cyclin D1, cyclin E1 and Bcl-2 (P<0.05) in a dose-dependent manner. However, these effects induced by Dio were inhibited by GW9662 (P<0.05), a specific inhibitor of PPARγ. CONCLUSION:Dio may inhibit proliferation and induce apoptosis in human glioblastoma U87MG cells most likely via up-regulating the expression of PPARγ, and then down-regulating the protein levels of cyclin D1, cyclin E1 and Bcl-2, and up-regulating the protein level of Bax. 相似文献
17.
AIM:To investigate the effects of sinapine, an effective monomer of Chinese medicine, on hydrogen peroxide (H2O2)-induced adipogenic differentiation of bone marrow mesenchymal stem cells (BMSCs).METHODS:The undifferentiated rat BMSCs were identified and screened by flow cytometry. The adipogenic differentiation of BMSCs was induced by H2O2, and the toxicity of sinapine on BMSCs was tested by CCK-8 assay. After the modeling method and the concentration range of sinapine were determined, the lipid droplets in the cells were detected by Oil Red O semi-quantitative assay, and the optimal drug concentration was selected. Finally, Oil Red O assay was observed 24 h after drug intervention, and the expression of adipogenic differentiation-related proteins, adipocyte protein 2 (aP2), peroxisome proliferator-activated receptor γ (PPARγ) and glucose transporter 4 (Glut4), at mRNA and protein levels in the BMSCs was determined by qPCR and Western blot.RESULTS:Treatment with H2O2 at 200 μmol/L for 1 h induced BMSCs to differentiate into adipocytes. Below the concentration of 40 μmol/L, sinapine had no toxicity to BMSCs. The best inhibitory concentration of sinapine on adipogenic differentiation was at 15 μmol/L. The number of lipid droplets in sinapine (15 μmol/L) group was significantly lower than that in model group. In sinapine group, the expression of aP2, PPARγ and Glut4 at mRNA and protein levels was lower than that in model group (P<0.01).CONCLUSION:Sinapine inhibits H2O2-induced adipogenic differentiation of rat BMSCs. The mechanism may be related to the PPARγ/AMPK signaling pathway. 相似文献
18.
CHEN Meng-yue CHEN Wei-dong LIU Yi-min XIANG Si-cheng YIN Hui-ling ZHANG Zhi-feng 《园艺学报》2019,35(1):106-111
AIM: To explore the effect of shikonin on rat primary cortical neurons in oxygen-glucose deprivation (OGD)-induced injury model.METHODS: The neurons were pretreated with shikonin at different concentrations (0.02, 0.2, 2 and 20 μmol/L) followed by treatment with OGD. Lactate dehydrogenase (LDH) release assay and fluorescein diacetate/propidium iodide (FDA/PI) double staining were used to detect neuronal viability and apoptosis, and then the optimal concentration of shikonin was determined. LY294002 (PI3K/Akt signaling pathway inhibitor, 1 μmol/L) was added before the addition of shikonin, and the protein level of p-Akt (Ser473) in the neurons was determined by Wes-tern blot. LDH release assay and FDA/PI double staining were also used to detect neuronal viability and apoptosis.RESULTS: A certain concentration (0.2~20 μmol/L) of shikonin increased the viability of impaired neurons (P<0.05) and the protein level of p-Akt (Ser473) in the neurons (P<0.05). The effect of shikonin on neuronal p-Akt (Ser473) levels and the cell death were blocked by LY294002 (P<0.05).CONCLUSION: A certain concentration of shikonin reduces OGD-induced apoptosis of rat primary cortical neurons by activating PI3K/Akt signaling pathway. 相似文献
19.
AIM: To investigate the effect of linarin (LIN) on the migration and invasion abilities of human breast cancer MDA-MB-231 cells and its underlying mechanism. METHODS: MCF-7, MDA-MB-231 and MCF-10A cells were cultured in vitro and treated with LIN at 5, 10, 20, 40, 80 and 160 μmol/L for 24 h, and the cell proliferation was measured by CCK-8 assay and colony formation assay. The protein levels of Snail, E-cadherin, matrix metalloproteinase-9 (MMP-9), IκBα, p-IKKα/β and p-p65 were determined by Western blot. RESULTS: LIN remarkably reduced the viability of MDA-MB-231 cells in a dose-dependent manner (P<0.05), and the IC50 was 55.89 μmol/L for 24 h. LIN decreased the colony formation rate of MDA-MB-231 cells at the concentration of 20 μmol/L (P<0.05). After exposed to LIN at 5 μmol/L and 10 μmol/L for 24 h, the migration and invasion abilities of the MDA-MB-231 cells were significantly reduced (P<0.05), the protein expression levels of E-cadherin and IκBα were up-regulated (P<0.05), the protein expression levels of Snail and MMP-9 were down-regulated (P<0.05), and the phosphorylation levels of IKKα/β and p65 were decreased (P<0.05) in comparison with the control group. Meanwhile, IKK-16 (IKKα/β inhibitor) and PDTC (NF-κB inhibitor) also down-regulated the protein expression levels of Snail and MMP-9 (P<0.05), and up-regulated the protein expression level of E-cadherin (P<0.05). CONCLUSION: LIN down-regulates the protein expression levels of Snail and MMP-9, and up-regulates the protein expression level of E-cadherin most likely through inhibiting IKK/NF-κB signaling pathway, and ultimately lead to decreases in the migration and invasion abilities of MDA-MB-231 cells. 相似文献
20.
AIM: To investigate the role of Herceptin in the apoptosis and drug sensitivity of endometrial cancer Ishikawa cells.METHODS: The IC50 values of Herceptin, adriamycin(ADR), cisplatin(DDP) and paclitaxel(PTX) for Ishikawa cells were detected by MTT method. Ishikawa cells were treated with single drug and combined chemotherapy for 24 h, the cell cycle and the apoptosis ratio were determined by flow cytometry.RESULTS: The IC50 values of Herceptin, ADR, DDP and PTX were 57.12 mg/L, 0.572 μmol/L, 67.4 μmol/L and 719.5 nmol/L, respectively. Herceptin significantly enhanced the cytotoxicity of the chemotherapeutic drugs, and increased apoptosis ratio statistically.CONCLUSION: Herceptin enhances the apoptosis-inducing ability of the chemotherapeutic drugs and improves the chemotherapeutic sensitivity in Ishikawa cells. 相似文献