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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
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AIM: To investigate the effect of shikonin on reversing hepatocyte growth factor(HGF)-induced resistance to gefitinib in lung cancer HCC827 cells, and to explore its possible mechanisms.METHODS: The gefitinib-resistant HCC827 cells induced by HGF were treated with shikonin and gefitinibthe alone or in combination. The inhibition rates of cell viability were determined by MTT assay. The invasive ability of HCC827 cells with HGF-induced resistance to gefitinib was determined by Transwell assay. The protein levels of epithelial-mesenchymal transition (EMT) and related signaling pathway in the HCC827 cells were detected by Western blot.RESULTS: The results of MTT assay showed that the cell activity of HCC827 cells was significantly inhibited by shikonin in a dose dependent manner. The IC50 of shikonin in HCC827 cells was 3.06 μmol/L. And the IC50 of gefitinib in HCC827 cells was 0.51 μmol/L. Under the condition of combined treatment with shikonin and gefitinib in the presence of HGF (20 μg/L), the IC50 of gefitinib was 7.36 μmol/L, significantly lower than that treated with gefitinib alone (P<0.01), so did the result of the cell migration (P<0.01). HGF induced EMT, while shikonin reversed this effect. The protein expression level of p-AKT was significantly up-regulated by HGF, while markedly down-regulated treatment with shikonin and gefitinib compared with gefitinib alone (P<0.01).CONCLUSION: Shikonin reverses HGF-induced resistance to gefitinib in lung cancer HCC827 cells, and the mechanism may be likely related to the preventon of EMT and the inhibition of HGF-induced activation of p-AKT signaling pathway. 相似文献
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AIM:To investigate the effect of shikonin on the apoptosis and oxidative stress induced by high concentration of glucose in vascular endothelial cells. METHODS:Rat thoracic aortic endothelial cells were randomly divided into 5 groups:normal control group (with glucose at concentration of 5.5 mmol/L in cell culture medium), high glucose group (with glucose at concentration of 33 mmol/L in cell culture medium), high glucose+low shikonin group (with glucose at concentration of 33 mmol/L and shikonin at concentration of 0.1 μmol/L in cell culture medium), high glucose+medium shikonin group (with glucose at concentration of 33 mmol/L and shikonin at concentration of 1 μmol/L in cell culture medium), and high glucose+high shikonin group (with glucose at concentration of 33 mmol/L and shikonin at concentration of 10 μmol/L in cell culture medium). After treatments, the cell viability was measured by CCK-8 assay and cell apoptotic rate was analyzed by flow cytometry. In addition, the status of oxidative stress was evaluated by determining the levels of malondialdehyde (MDA), reactive oxygen species (ROS), superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px). The activation of Nrf2/HO-1 signaling pathway was determined by Western blot. RESULTS:Compared with high glucose group, shikonin reversed high glucose-induced decrease in cell viability and increase in apoptosis in a concentration-dependent manner. High concentration of glucose induced high levels of MDA and ROS, while decreased the levels of SOD and GSH-Px. However, after treatment with shikonin, the contents of MDA and ROS were decreased, while the activities of SOD and GSH-Px were increased as compared with high glucose group. Furthermore, the high concentration of glucose up-regulated the protein levels of cleaved caspase-3, HO-1 and Nrf2 (nuclear). Compared with high glucose group, the protein levels of cleaved caspase-3, HO-1 and Nrf2 (nuclear) were partly decreased after treatment with shikonin. CONCLUSION:Shikonin alleviates high glucose-induced vascular endothelial cell apoptosis. Its mechanism may be related to activation of Nrf2/HO-1 signaling pathway and down-regulation of oxidative stress in vascular endothelial cells. 相似文献
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紫草愈伤组织培养中紫草素形成的影响因素 总被引:7,自引:0,他引:7
采用两阶段培养法研究不同培养基,激素的种类,浓度和各种营养成分对愈伤组织生长及紫草素形成的影响。结果表明,改良B5培养为适宜的营养生长培养基,细胞分裂素和生长素均为紫草素形成所必要的。6-BA1.0mg.L^-1,IAA0.1mg.L^-1为较佳配比,生长培养基中CaCl2浓度为250mg.L^-1,MgSO4为500mg.L^-1时,愈伤组织生长和紫草素形成均较佳,紫草素形成培养其中CuSO4为M9浓度的3倍时,紫草素产量较高,紫草不形成培养其中添加VB2及更高的FeSO4对紫草素产量的提高没有效果,研究过程中优化了草细胞培养成草草素的方法,为建立完善整的组培生产紫草素体系提供了基础数据。 相似文献
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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
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AIM:To explore the reversal effect of shikonin on cisplatin resistance of ovarian cancer SKOV3/DDP cells and its potential mechanism. METHODS:The proper conditions of treatment with shikonin and cisplatin were determined by CCK-8 assay. The cell cycle and apoptotic rate were analyzed by flow cytometry. The protein levels of cell cycle-and apoptotic-related molecules, such as cyclin D1, cyclin-dependent kinases 2 (CDK2), P18, p-Rb, Bcl-2, Bax and cleaved caspase-3, were determined by Western blot. RESULTS:The results of CCK-8 assay showed that compared with cisplatin group, combined treatment with shikonin and cisplatin had a better inhibitory effect on the growth of cisplatin-resistant SKOV3/DDP cells. The cell cycle G1/S transition was inhibited, while early apoptotic rate was increased after combined use of shikonin and cisplatin. The results of Western blot showed that compared with cisplatin group, the cells in combination group had lower protein levels of cyclin D1, CDK2, p-Rb and Bcl-2, accompanied with higher protein levels of P18, Bax and cleaved caspase-3. CONCLUSION:Shikonin reverses the cisplatin resistance of ovarian cancer SKOV3/DDP cells. The mechanism may be related to the regulation of cell cycle-and apoptotic-related molecules, and further inhibition of cell viability and promotion of cell apoptosis. 相似文献
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Preparation of shikonin by hydrolyzing ester derivatives using basic anion ion exchange resin as solid catalyst 总被引:1,自引:0,他引:1
Ting-ting LiuChun-hui Ma Xiao-yu SuiLei Yang Yuan-gang Zu Chun-jian ZhaoChun-ying Li Lin Zhang 《Industrial Crops and Products》2012,36(1):47-53
An efficient catalytic hydrolysis approach was developed to prepare shikonin from its ester derivatives with anion exchange resins as solid catalyst. The performance of seven anion exchange resins including D290, D296, D261, D280, 201×7, D301-G and D301-R has been evaluated. The research results indicate that D290 resin is the most appropriate for preparation of shikonin. The reaction conditions such as reaction temperature, reaction time, catalyst amount and catalyst reuse have been studied. The maximum yield of shikonin reached 93.74 ± 2.99% under optimal conditions of hydrolysis temperature 20 °C, hydrolysis and desorption time both 30 min and resin amount 10% (w/v). HPLC chromatograms of samples, obtained after the new catalytic process, demonstrated that conversion of shikonin ester derivatives into shikonin performed well. 相似文献