共查询到19条相似文献，搜索用时 62 毫秒
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目的：探讨姬松茸多糖（Agaricus blazeiMuril lPolysac．charides,ABPS）对体外高糖培养乳鼠心肌细胞凋亡的抑制作用及其机制。方法：将Wistar乳鼠原代细胞随机分为5组,A：空白对照组;B：高糖组;C：0．4mg／mLABPS组;D：0．8mg／mLABPS组。用荧光显微镜测定各组细胞凋亡情况,RT—PCR法检测bcl-2、caspase-3基因表达量的变化。结果：经ABPS干预后,凋亡细胞明显减少,bcl-2表达增加,caspase～3表达减少。结论：ABPS抑制体外高糖培养的乳鼠心肌的凋亡,其机制可能与抑制caspase-3、激活bcl-2表达有关。 相似文献
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木蹄层孔菌子实体提取物体外抑菌活性研究 总被引：3，自引：0，他引：3
首次采用滤纸扩散法和平板涂布法对木蹄层孔菌Fomes fomentarius（L：Fr．）Kick．子实体的水、甲醇、丙酮、乙酸乙酯、氯仿、石油醚等提取物进行了抑菌活性研究。结果表明,木蹄层孔菌各提取物对白色念珠菌JLC31680、白色念珠菌JLC31681、大肠杆菌ATCC 8099、金黄色葡萄球菌ATCC6538均有不同程度的抑制作用。其中水提物与其他5个提取物相比,对金黄色葡萄球菌ATCC6538的抑制作用最强,其次对大肠杆菌ATCC8099,当浓度为100mg·mL^-1时,抑制率分别为95．54％和73．80％,最小抑菌浓度（MIC）分别是50mg·mL^-1、25mg·mL^-1。对白色念珠菌JLC31680和白色念珠菌JLC31681的抑制作用也较为明显,当浓度为100mg·mL^-1时,抑菌率分别为33．06％和26．67％,最小抑菌浓度（MIC）分别是12．5mg·mL^-1、50mg·mL^-1。甲醇提取物与其他5个提取物相比,对大肠杆菌ATCC8099和金黄色葡萄球菌ATCC6538的抑制作用最强,当浓度为50mg·mL^-1时,抑菌率分别为99．39％和95．10％,最小抑菌浓度（MIC）是12．5mg·mL^-1、25mg·mL^-1,且均有量效关系。 相似文献
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樟芝(Taiwanofungus camphoratus)发酵液和经95％乙醇浸提后的菌丝体醇提物分别用石油醚和氯仿进行分级提取,得到石油醚和氯仿提取物.对不同提取物进行体外抑制SPCA-1肺癌细胞增殖实验,发现各提取物均可抑制SPCA-1细胞的增殖,其中发酵液石油醚提取物抑制作用最好,IC5.为62.5 μg/mL,发酵液和菌丝体氯仿提取物的抑制作用较好,IC50分别为120.9和109.5 μg/mL,菌丝体石油醚提取物的抑制作用较差,在25～150 μg/mL作用浓度下,抑制率低于20％.各提取物对SPCA-1细胞凋亡和生长周期作用的测定结果表明,各提取物在肺癌细胞SPCA-1中通过诱导细胞凋亡及S期周期阻滞来表现其抑制作用. 相似文献
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以肿瘤细胞HepG2、B16、K562和正常细胞WPMY-1为受试细胞,对棘托竹荪(Dictyophora echinovolvata)发酵菌丝体和发酵液不同浓度乙醇提取物和水提物的体外抗肿瘤活性进行测定.结果表明:菌丝体的不同乙醇浓度提取物仅对肿瘤细胞K562和B16的增殖有较好的抑制作用,而在实验浓度内对肿瘤细胞HepG2和正常细胞WPMY-1增殖的抑制能力较弱.与菌丝体相比,发酵液对肿瘤细胞的增殖抑制作用更强,其不同浓度乙醇提取物对肿瘤细胞HepG2、B16、K562和正常细胞WPMY-1的增殖都有较强的抑制能力. 相似文献
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为评价茯苓(Poria cocos)多糖对非小细胞肺癌NCI-H460细胞的抑制作用,用CCK-8法测定茯苓多糖对细胞增殖的抑制率,用DAPI染色法、AOEB双荧光染色法分析茯苓多糖对细胞凋亡的影响,用细胞划伤愈合实验测定茯苓多糖对细胞迁移能力的影响,用蛋白免疫印迹实验检测茯苓多糖对细胞凋亡、迁移相关蛋白表达的影响。结果表明：茯苓多糖具有抑制NCI-H460细胞增殖、集落形成和迁移的能力,可诱导NCI-H460细胞凋亡;500、1 000μg·mL-1的茯苓多糖可使Bax和P53蛋白表达量升高,Bcl-2和MMP-2蛋白表达量降低。 相似文献
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虫草液体深层发酵富硒的研究 总被引：5，自引：0，他引：5
研究了不同硒浓度、培养时间、pH、培养基种类等因素对虫草菌丝体生长量、富硒量、有机硒转化率的影响，探讨了虫草菌富硒的最优培养条件。结果表明其最优富硒培养条件为：培养基硒浓度60μg／mL，培养时间5d，pH6，培养基为麸皮培养基（％）：蔗糖3，麸皮2，NaN030．2，KH2V040．5。菌丝生长量最高可达1．916g/100mL，有机硒含量可达509．026μg／100mL。虫草有机硒转化率最佳培养条件为：培养基硒浓度20μg／mL，培养时间5d，pH7，培养基为马铃薯培养基（％）：蔗糖3，马铃薯20，NaNCh0．2，KH2PO40．5。其有机硒转化率最高可达18．44％。低浓度的硒可以刺激菌丝体生长，高浓度的硒对菌丝体生长有抑制作用，使有机硒转化率降低。 相似文献
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AIM: To probe into the role of 1, 4, 5-trisphosphate inositol (IP3) and survivin protein in apoptosis of HepG2 cells induced by genistein. METHODS: HepG2 cells were treated with 60 μmol/L genistein for 12 h, 24 h, 48 h and 72 h. IP3, survivin and apoptosis rate were assayed by IP3-［3H］ Birtrak assay, Western blotting and flow cytometry, respectively. RESULTS: IP3 in groups incubated for 12 h, 24 h, 48 h and 72 h with 60 μmol/L genistein were significantly lower than that in control (P<0.01) ［(12.0±1.4) pmol/106cells, (7.5±0.8) pmol/106 cells, (5.6±0.5) pmol/106cells, (3.3±0.6) pmol/106 cells， vs (29.2±0.6) pmol/106 cells］. V-survivin/ V-β-actin, which was the gray degree multiply area of survivin/the gray degree multiply area of β-actin in groups incubated for 12 h, 24 h, 48 h and 72 h with 60 μmol/L genistein, were significantly lower than that in control (P<0.01) ［（0.36±0.13, 0.33±0.03, 0.23±0.04, 0.18±0.04）， vs 0.63±0.06］. The apoptosis rate in groups incubated with 60 μmol/L genistein for 24 h, 48 h and 72 h was significantly higher than that in control （P<0.01） ［(7.4%±0.5%, 20.5%±2.0%, 30.7%±1.6%) vs 2.6%±0.1%］. CONCLUSION: Genistein induces apoptosis in HepG2 cells by reducing IP3 production and survivin protein expression. 相似文献
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AIM: To investigate the effects of artesunate on proliferation and apoptosis in human hepatocelluar carcinoma cell line HepG2 and to study the sensitizing effect of artesunate on HepG2 cells to chemotherapeutic drugs. METHODS: The proliferation of HepG2 cells was determined by the assay of cell counting kit-8 (CCK-8) and the colony formation test. The morphology of HepG2 cells with Hoechst 33258 staining was observed under fluorescent microscope. Annexin V/propidium iodide (PI) was used to analyze the apoptosis and the cell cycle. The sensitizing effects of artesunate on HepG2 cells to chemotherapeutic drugs were determined by CCK-8 assay. RESULTS: When treated with artesunate for 48 h, the proliferation of HepG2 cells was significantly inhibited in a dose-dependent manner. The IC50 was 19.2 μmol/L. Compared with the control cells, the colony formation of HepG2 cells treated with artesunate for 7 days was significantly inhibited. The nuclear fragmentation, karyopyknosis, chromosomal condensation, cell shrinkage, and attachment loss in HepG2 cells treated with artesunate were observed. The cells in G2 phase increased obviously, and the percentages of hypodiploid cells and early apoptotic rates were significantly higher in artesunate treatment groups than those in control group. The IC50 of 5-FU, carboplatin and epirubicin combined with artesunate was 3.33, 2.02 and 1.71 times sensitized as compared with control group, respectively. CONCLUSION: Artesunate effectively inhibits proliferation and induces apoptosis of HepG2 cells. Aresunate also sensitizes HepG2 cells to chemotherapeutic drugs. 相似文献
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HAI Guang-fan NIU Bing-xuan LI Pin-pin GUO Lan-qing CUI Tai-zhen LI Sheng-ying 《园艺学报》2014,30(10):1879-1882
AIM:To investigate the effects of nodosin extracted from Chinese traditional medicine on the proliferation of HepG2 cells cultured in vitroand to detect the protein expression of Bcl-2 and Bax in HepG2 cells. METHODS:HepG2 cells were treated with different concentrations (1.25, 2.5, 5, 10 and 20 μmol/L) of nodosin for 24 h. The morphological changes of HepG2 cells were observed under inverted microscope. The inhibitory rates of HepG2 cell growth were detected by MTT assay. The apoptotic rates and the protein expression of Bcl-2 and Bax were analyzed by flow cytometry. RESULTS:Shrunken and suspended HepG2 cells increased with the increases in the concentrations of nodosin. The apoptotic rates and the expression of Bax increased with the increases in the doses of nodosin, while the expression of Bcl-2 decreased. CONCLUSION: Nodosin inhibits the growth of HepG2 cells in a dose-dependent manner. The inhibition of HepG2 cell growth is induced by decreasing Bcl-2 and increasing Bax, thus promoting cell apoptosis. 相似文献
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AIM: To investigate the proliferation-inhibitory and apoptosis-inducing effects of harmine on human hepatocarcinoma HepG2 cells. METHODS: The proliferation of HepG2 cells was determined in the absence or presence of a JNK inhibitor SP600125 by Cell Counting Kit-8 (CCK-8) assay and colony formation test. The morphology of HepG2 cells was observed by Hoechst 33258 staining under fluorescence microscope. The cell apoptosis was analyzed by Annexin V-PI staining. The expression of apoptosis-regulated proteins,poly(ADP-ribose) polymerase (PARP),c-Jun N-terminal kinase (JNK) and p-JNK, was detected by Western blotting. The sensitizing effects of harmine on HepG2 cells to chemotherapeutic drugs 5-fluorouracil (5-FU) and cisplatin were determined by CCK-8 assay. RESULTS: Harmine inhibited the proliferation of HepG2 cells and induced apoptosis in a dose-dependent manner. After the JNK signaling pathway was blocked by SP600125, the cell apoptotic rate decreased significantly. Hoechst 33258 staining revealed that the nuclear fragmentation, chromosomal condensation, cell shrinkage and attachment loss appeared in the HepG2 cells treated with harmine. The percentage of the sub-G1 fraction was increased and the population of early apoptotic cell death was observed. Apoptosis of HepG2 cells with harmine treatment was associated with the activation of JNK. Combined with harmine, the IC50 values of 5-FU and cisplatin for the tumor cells were 1.47 and 5.78 times sensitized as compared with the correspon-ding single drug treatment groups, respectively. CONCLUSION: Harmine exhibits an anti-proliferative effect on HepG2 cells by inducing apoptosis. The JNK signaling pathway is involved in the apoptosis of HepG2 cells. Harmine enhances the chemosensitivity of the cells to 5-FU and cisplatin. 相似文献
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AIM: To determine whether caudatin, a C21 steroidal aglycone, enhances tumor necrosis factor-related apoptosis-inducing ligand(TRAIL)-associated HepG2 cell apoptosis. METHODS: Cell growth inhibition was determined by MTT assay and cell colony formation assay. The TUNEL apoptosis detection kit was used to analyze cell apoptosis, and the protein expression was examined by Western blotting. RESULTS: Combination of caudatin with TRAIL signi-ficantly reduced cell proliferation and increased the apoptotic rate of HepG2 cells compared with the use of each agent alone. This was evidenced by marked increases in caspase-3, caspase-7, caspase-9 and PARP cleavages in the cells treated with caudatin and TRAIL-compared with control group. Combination of caudatin with TRAIL also led to the strong suppression of survivin. CONCLUSION: Caudatin synergizes HepG2 cells to TRAIL-induced apoptosis by promoting the cleavages of caspase-3, caspase-7, caspase-9 and PARP and inhibiting the expression of survivin. 相似文献
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AIM To investigate the effect of sinomenine （SIN） on the apoptosis of human rheumatoid arthritis （RA） fibroblast-like synoviocytes （FLS） and its molecular mechanism. METHODS Human RA FLS were isolated and cultured. The cells treated with lipopolysaccharide （LPS） at 100 mg/L was recorded as LPS group. The cells treated with SIN at 3.2 mmol/L and LPS at 100 mg/L were recorded as LPS+SIN group. The cells without any treatment served as blank group. The cells transfected with miR-con, miR-23b-3p, si-con and si-fibroblast growth factor 9 （FGF9） and treated with 100 mg/L LPS were recorded as LPS+miR-con group, LPS+miR-23b-3p group, LPS+si-con group and LPS+si-FGF9 group, respectively. The anti-miR-con, anti-miR-23b-3p, pcDNA and pcDNA-FGF9 were also transfected into RA FLS, and then the cells were treated with SIN at 3.2 mmol/L and LPS at 100 μg/mL. These cells were recorded as LPS+SIN+anti-miR-con group, LPS+SIN+anti-miR-23b-3p group, LPS+SIN+pcDNA group, LPS+SIN+pcDNA-FGF9 group, respectively. The cell viability was measured by CCK-8 assay. The number of colonies was accessed by colony formation experiment. The protein levels of FGF9, cleaved caspase-3, Bax and Bcl-2 were determined by Western blot. The apoptosis was analyzed by flow cytometry. The expression of miR-23b-3p and FGF9 mRNA was detected by RT-qPCR. Dual-luciferase reporter assay was used to verify the targeting relationship between miR-23b-3p and FGF9. RESULTS Treatment with SIN promoted LPS-induced apoptosis of RA FLS, inhibited cell proliferation, up-regulated miR-23b-3p expression, and down-regulated FGF9 expression. miR-23b-3p targeted FGF9. Over-expression of miR-23b-3p or silencing of FGF9 inhibited LPS-induced proliferation and enhanced apoptosis of the RA FLS. Interfering with miR-23b-3p or over-expression of FGF9 reversed the effects of SIN on the proliferation and apoptosis of LPS-induced RA FLS. CONCLUSION Sinomenine induces RA FLS apoptosis and inhibits cell proliferation through miR-23b-3p/FGF9 signaling. 相似文献
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AIM: To study the mechanism of oleanolic acid induced apoptosis and its influence on cell cycle in HL-60 cells in vitro. METHODS: The HL-60 cells were treated with different concentrations of oleanolic acid and then cultured for 12 h, 24 h, 48 h and 72 h, respectively. MTT assay was used to evaluate the inhibitory effect of oleanolic acid on HL-60 cells in vitro. The argarose gel electrophoresis was used to detect the chromatin DNA fragmentation. FACS was used to analyze the cell cycle of HL-60 cells. Western blotting was used to detect the activation of caspase-3 which has been confirmed the last execution of apoptosis pathway. RESULTS: MTT assay showed that oleanolic acid dramatically inhibited the growth of HL-60 cells in vitro, more than 50% HL-60 cells were inhibited when the cells were treated with 80 μmol/L oleanolic acid for 48 h; the apparent DNA ladder was detected after exposure of HL-60 cells to oleanolic acid for 48 h. FACS analysis showed that cell cycle of HL-60 cells was arrested in G1 phase, the inhibition ratio of HL-60 cells achieved 63.24% and 67.90% after treated with oleanolic acid for 48 h and 72 h correspondingly. Western blotting detected the activation of caspase-3 after exposure of HL-60 cells to 80 μmol/L oleanolic acid for 48 h. CONCLUSION: These results suggest that oleanolic acid induces apoptosis and the cell cycle of HL-60 cells is arrested in G1 phase. 相似文献
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AIM To explore the effect of dasatinib on the viability, apoptosis and migration of human renal carcinoma cell lines 786-O and 769-P, as well as the molecular mechanism in vitro . METHODS 786-O cells and 769-P cells were treated with different concentrations （0~2 μmol/L） of dasatinib, and 0 μmol/L dasatinib was used as blank control group. MTT method was used to detect cell viability. Wound healing assay was used to detect the effect of dasatinib on migration. Hoechst 33258 staining was used to observe the effect of dasatinib on apoptosis. Flow cytometry was used to detect the effect of dasatinib on cell cycle. Western blot method was used to detected cell cycle- and apoptosis-related protein levels. RESULTS Dasatinib inhibited viability and migration of 786-O and 769-P cells, and the inhibitory effect of dasatinib increased with the concentration of dasatinib （P <0.05）. The IC50 values of dasatinib against 786-O and 769-P cell lines were （0.958 7±0.028 8） μmol/L and （0.784 3±0.066 0） μmol/L, respectively. After treatment with dasatinib for 24 h, the expression of pro-apoptotic proteins cleaved caspase-3 and cleaved caspase-9 increased significantly （P <0.01）, while the expression of cyclin D1 decreased （P <0.05）. The cycle-related pathway proteins p53 and p21 increased （P <0.05）, while the level of p-AKT was decreased （P <0.05）. CONCLUSION Dasatinib impaired the viability and migration ability of human renal carcinoma cell lines 786-O and 769-P by up-regulating p53 expression and down-regulating AKT phosphorylation. 相似文献