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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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毛蜂窝菌提取物体外抗肿瘤活性的研究 总被引：1，自引：0，他引：1
以人肺癌细胞NCI-H460、中枢神经系统癌细胞SF-268及乳腺癌细胞MCF-7为供试细胞株,采用MTT(四甲基偶氮唑盐)法对毛蜂窝菌(Hexagona apiaria)野生子实体、栽培子实体、培养废料、发酵菌丝体的醇提物和发酵液乙酸乙酯萃取物、发酵液水相部分等各提取物进行了体外抗肿瘤活性研究.结果表明,毛蜂窝菌发酵液乙酸乙酯萃取物对三种肿瘤细胞株都有较明显的抑制作用,抑制率达80%以上;其它提取物也有一定的抑制作用,但抑制率在40%以下. 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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茯苓的发酵研究及其动物免疫学观察 总被引：9，自引：0，他引：9
研究表明 ,茯苓发酵培养经 0 - 48h的适应期 ,48- 144h的增殖生长期后进入稳定生长期 ,并出现pH值骤降 ,经检测 ,发酵液中含有包括十六烷酸和十八烷酸在内的有机酸 ;发酵罐培养在 12 0h生物量可达到 30g/10 0ml (鲜重 )以上 ;提取茯苓营养浓缩液多糖含量≥5 0mg/ml,氨基酸含量≥ 480mg/ 10 0ml,经动物试验证明 ,其具有显著提高机体免疫力的作用 ,重金属及微生物指标符合国家标准。 相似文献
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《北方园艺》2020,(10)
为了探究解无机磷细菌B51-7最佳发酵培养条件,以发酵液初始pH、碳源、氮源和培养温度为研究对象,以钼蓝比色法测定发酵液中可溶性磷含量为评价指标,通过单因素试验和正交实验确定其发酵条件的最佳组合。结果表明:初始pH 4.5、30℃、10 g·L~(-1)葡萄糖、0.1 g·L~(-1)蛋白胨培养条件下,菌株B51-7发酵液中可溶性磷含量最高;菌株B51-7解磷能力的最优发酵条件组合为初始pH 4.0,葡萄糖12 g·L~(-1),蛋白胨0.05 g·L~(-1),温度30℃。该研究为菌株B51-7解磷能力的掌握以及其在微生物磷肥的开发与利用提供了重要的参考依据。 相似文献
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《中国食用菌》2015,(3)
研究长柄侧耳发酵液对高脂饮食小鼠血脂的影响,以及护肝和抗氧化的作用。通过高脂饮食建造小鼠高脂模型,同时以长柄侧耳发酵液灌胃给药,生理盐水作为空白对照,脂必妥片作为阳性对照。连续灌胃45 d后,测定甘油三酯(TG)、总胆固醇(CHO)、高密度脂蛋白(HDLC)、低密度脂蛋白(LDLC)、谷草转氨酶(AST)、谷丙转氨酶(ALT)、总超氧化物歧化酶(T-SOD)、丙二醛(MDA)、微量还原型谷胱甘肽(GSH)含量。发酵液组较模型组TG、CHO、LDLC、ALT、AST、MDA、GSH含量均有不同程度降低;HDLC、SOD含量有不同程度提高。长柄侧耳发酵液可以预防由高脂饮食造成的小鼠高脂血症,同时具有保护肝脏和抗氧化作用。 相似文献
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《中国南方果树》2021,(3)
为丰富香蕉枯萎病生防菌资源,探究其抑菌机理,从润楠Machilus pingii根系土壤中分离筛选对香蕉枯萎病菌具有拮抗作用的放线菌,基于16S rRNA序列进化分析和生理生化特征,鉴定其种属。利用激光共聚焦显微镜评测盆栽试验的防控效果,并通过扫描电镜、透射电镜分析其对枯萎病菌孢子形态结构及超微结构的影响。结果表明,试验筛选出1株拮抗效果较好的放线菌,鉴定为链霉菌属,命名为JRGG-11。该菌对枯萎病菌4号生理小种(Foc 4)的抑菌率为(80.48±1.49)%,发酵液的抑菌率为(58.77±1.31)%,发酵液对Foc 4的盆栽防控效果为83.10%。菌株JRGG-11提取物对Foc 4菌丝生长抑制的EC_(50)为18.70μg/mL,当用4×EC_(50)处理时,Foc 4菌丝形态和细胞完整性被严重破坏,孢子萌发完全被抑制。说明链霉菌JRGG-11具有较好的生防潜能。 相似文献
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AIM:To investigate the signal transduction mechanism of rapid effect of corticosterone. METHODS:With liquid scintillation technique, the effect of corticosterone on glycine uptake in C6 cells was examined. RESULTS: The bovine serum album in coupled with corticosterone had the same effect as corticosterone 21-sulfate(B); Neomycin partially blocked the effect of B in C6 cells; GDP-β-S attenuated the effects of B on glycine uptake in C6 cells; Chelerythrine chloride (Chelery) partially blocked the effect of B in C6 cells; H89 had no influence on the effect of B in C6 cells. The Km and Vmax of effect of B on glycine uptake in C6 cells were different from those in SK-N-SH cells. CONCLUSION:PKC, instead of PKA, was involved in the signal transduction of the rapid effect of B on glycine uptake in C6 cells. The converse effects of B on C6 cells and SK-N-SH cells resulted from different transportation system in two kinds of cells. 相似文献
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WANG Qing SONG Li-juan LI Yan-hua YANG Zhi-chao WANG Jing LIU Jian-chun JIANG Wei-jia MA Cun-gen 《园艺学报》2018,34(8):1486-1490
AIM: To investigate the different inhibitory effects of proanthocyanidins B1 and B2, which are isomers, on the inflammatory response of BV-2 cells induced by lipopolysaccharide (LPS). METHODS: MTT assay was used to detect the effects of proanthocyanidins B1 and B2 on the viability of BV-2 cells. LPS (1 mg/L) was used to promote BV-2 cells to secrete inflammatory factors. ELISA, chemotaxis assay and Western blot were used to detect the influence of proanthocyanidins B1 and B2 on the levels of tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), cell chemotaxis and phosphorylation of NF-κB. RESULTS: Proanthocyanidins B1 and B2 did not show cytotoxicity effect on BV-2 cells. Proanthocyanidin B1 and B2 inhibited the cell chemotaxis, phosphorylation of NF-κB, and releases of TNF-α and IL-1β. CONCLUSION: Proanthocyanidins B1 and B2 inhibit the inflammatory response of BV-2 cells induced by LPS, and their action intensity didn't show significant difference. 相似文献
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DENG Chun-yan ZHANG Guo-chao DENG Shao-ping REN Li-li JIANG Jin-xing YU Li-na QI Hui LI Fu-rong 《园艺学报》2016,32(3):492-498
AIM: To investigate the role of B cells in CD45RB antibody-induced transplantation immune tolerance. METHODS: Single cell suspension was made from the spleen of BALB/c nude mice disposed by CD45RB antibody, then mixed cultured with T cells of BALB/c mice and spleen cells of C57BL/6 mice. The Th1, Th2, Treg and Tm cells were monitored by flow cytometry during the culture process. The skin graft model was set up with B6.μMT-/- mice as receptors and BALB/c mice as donors. CD45RB antibody was intraperitoneally injected into the receptors after transplantation and then CD3+CD45RBhi cells were detected by flow cytometry. In another mixed lymphocyte culture, CD45RB antibody was added, and then B cells were isolated and injected into B6.μMT-/- mice through the tail vein. The heart transplantation model was established with B6.μMT-/- mice as receptors and BALB/c mice as donors, and then the survival and the migration of B cells to the thymus were observed. RESULTS: When T lymphocytes were co-cultured with B lymphocytes treated with anti-CD45RB monoclonal antibody(mAb) in vivo, the percentages of Th2 and Treg cells were up-regulated and Th1 cells were down-regulated, but Tm cells were not altered as compared with the control. In vivo without B lymphocytes, anti-CD45RB mAb also down-regulated the expression of CD45RB in T lymphocytes. The reduction was faster and the percentage of CD3+CD45RBhi T cells was not altered as compared with the control. The B lymphocytes treated with anti-CD45RB mAb in vitro prolonged the lifetime of receptor in heart transplantation model but failed to induce complete tolerance. After recieving B cells treated with anti-CD45RB mAb and allogeneic heart transplantation, B cells migrated to the thymus in B6.μMT-/- mice. CONCLUSION: B lymphocytes play a definite role in the transplantation immune tolerance induced by anti-CD45RB mAb through their affection on T-cell subgroups and also in the central tolerance. However, the induction of immune tolerance can not only rely on B cells. 相似文献
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AIM: To detect the expression of WNT5B in normal breast epithelial cells and different breast cancer cell lines, and to investigate the effects of WNT5B over-expression on the viability and apoptosis of human breast cell line MCF-7.METHODS: The mRNA expression of WNT5B was detected by RT-PCR in different breast cancer cells. MCF-7 cells were transfected with plasmid pcDNA3.1/WNT5B or pcDNA3.1, and the expression of WNT5B at mRNA and protein levels was examined in the 2 groups by real-time PCR and Western blotting, respectively. Subsequently, the changes of cell viability and cell apoptosis were analyzed by CCK-8 assay and flow cytometry, respectively. RESULTS: The expression of WNT5B in the breast cancer cell lines was lower than that in MCF10A cells. The WNT5B expression in the MCF-7 cells in experimental group was significantly higher than that in vector group (P<0.05). However, the cell viability in experimental group decreased significantly as compared with vector group (P<0.05). The number of the cells in S-phase obviously increased, while the percentage of the cells in G1-phase and G2/M-phase decreased compared with vector group. The number of apoptotic cells in WNT5B group was significantly higher than that in vector group.CONCLUSION: The expression of WNT5B is decreased in breast cancer cells. WNT5B over-expression significantly inhibits the cell growth and promotes the cell apoptosis in breast cancer MCF7 cells. 相似文献
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AIM: To detect the endogenous expression of B-cell leukemia/lymphoma 6 member B (BCL6B) in FHC and LoVo cells, and to investigate the effects of BCL6B on proliferation and migration of LoVo cells for further exploring the underlying mechanism. METHODS: The endogenous expression of BCL6B in the FHC and LoVo cells was detected by RT-PCR and Western blot. The methods of MTT assay, colony formation assay, wound healing assay and Transwell chamber experiment were employed to examine the biological functions of BCL6B in the LoVo cells. The mRNA and protein levels of BCL6B, cyclin D1 and matrix metalloproteinase-9 (MMP-9) were determined by RT-PCR and Western blot, respectively. The level of phosphorylated protein kinase B (p-AKT) was detected by Western blot. RESULTS: BCL6B expression was notably repressed in the LoVo cells as compared with the FHC cells, which were significantly increased by transfection with pcDNA3.1-BCL6B. The abilities of proliferation and migration of the LoVo cells at 72 h were inhibited by 28.33%(P<0.01) and 36.11%(P<0.05) in BCL6B group. The mRNA levels of cyclin D1 and MMP-9 in the cells of BCL6B group were decreased by 39.90%(P<0.01) and 77.36% (P<0.05), and the protein levels of cyclin D1, MMP-9 and p-AKT were reduced by 44.00%(P<0.05), 47.06%(P<0.01) and 32.88% (P<0.05), respectively. CONCLUSION: BCL6B inhibits proliferation and migration of the LoVo cells, and the PI3K/AKT signaling pathway is involved in this process. 相似文献
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AIM: To investigate the role of NF-κB in apoptosis induced by 10-hydroxycamptothecin (HCPT) in human breast carcinoma cells. METHODS: The cell growth inhibition was measured by MTT assay. Agarose gel electrophoresis was performed for cell apoptosis. Western blotting was performed for protein xpression. DIG-EMSA was conducted to determine the DNA-binding activation of NF-κB. RESULTS: HCPT had a remarkable effect of growth inhibition on breast cancer cells. After exposed to HCPT, the breast cancer cells presented some morphologic features of apoptosis including cell shrinkage, nuclear condensation and DNA fragmentation. NF-κB was activated in cancer cells treated with HCPT but not activated in IκBα-mutant cells and apoptosis was inhibited in IκBα-mutant cells treated with HCPT.CONCLUSION: HCPT may induce apoptosis and activation of NF-κB in a Bcap-37 cell line. Inhibition of NF-κB activation attenuates apoptosis induced by HCPT. 相似文献
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AIM:To optimize the IκBα mutant (IκBαM) gene derived from human placenta tissue by deleting N-terminal phosphorylation sites of serine 32/36,and to construct and identify its replication-deficient recombinant adenovirus (AdIκBαM).METHODS:The IκBαM gene (203-1 003 bp) was acquired by positional cloning,followed by subcloning it into pShuttle and pGEM-T vectors for further PCR,double digestion,DNA sequencing and homology analysis.Subsequently,the expression unit of pShuttle-IκBαM containing CMV promoter,IκBαM cDNA and poly A signals was inserted into Ad5 vector,after which the resultant recombinant adenovirus AdIκBαM was packaged in 293 cells by cotransfection with lipofectamine.Western blotting analysis and electrophoretic mobility shift assay were utilized to detect the AdIκBαM-mediated expression of IκBαM gene in 293 cells and its suppressive effect on phorbol myristate acetate (PMA)-induced nuclear factor κB (NF-κB) activation in ECV304 cells,respectively.RESULTS:The relevant nucleotide and amino acid sequence of IκBαM gene was consistent with that of GenBank (accession number M69043).The titer of the prepared AdIκBαM was 4.0×1012 pfu/L.Moreover,the IκBαM gene was expressed in 293 cells,and potently inhibited the PMA-induced NF-κB activation in ECV304 cells in a dose-dependent manner.CONCLUSION:AdIκBαM is a nonvel vector for both efficient transfer and expression of IκBαM gene as well as specific inhibition of NF-κB activity,providing a promising future for gene therapy of asthma. 相似文献
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AIM:To study the expression of murine interleukin-12(mIL-12) gene in B16F10 melanoma cells.METHODS:mIL-12 gene was inserted into pcDNA3.1 eukaryotic expression vector by DNA recombination and then transfected into B16F10 melanoma cells by electroporation. The integration and expression of mIL-12 gene in B16F10 melanoma cells were detected by PCR, RT-PCR and Western blot after positive cell clones had been screened.RESULTS:mIL-12 gene was confirmed to have been transfected and expressed in B16F10 cells on three levels of DNA, mRNA and protein.CONCLUSION:mIL-12 gene can successfully be transfected and expressed in B16F10 melanoma cells in vitro, which lays a foundation for the further investigation of mIL-12 gene tumor vaccine. 相似文献
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AIM To investigate the expression of histone chaperone anti-silencing function 1B （ASF1B） in prostate cancer cells and its effect on cell viability in vitro . METHODS Human prostate cancer PC-3 cells were used， and knockdown of ASF1B was conducted by small interfering RNA （siRNA） transfection into the cells. The cells were divided into control group， siRNA negative control vector （mock） group and siRNA-ASF1B group. The viability of the PC-3 cells treated with ASF1B-siRNA for 12， 24 and 48 h was measured by MTT assay. Flow cytometry was used to analyze cell apoptosis and cell cycle distribution. The mRNA expression of apoptosis-related molecules was detected by RT-qPCR， and the expression levels of MAPK/JNK/ERK signaling pathway-related proteins were determined by Western blot. RESULTS The protein level of ASF1B in the normal cells （benign prostatic hyperplasia） was significantly lower than that in the PC-3 cells （P <0.01）. Compared with control group and mock group， the protein expression level of ASF1B in the PC-3 cells transfected with siRNA-ASF1B plasmid and the viability of the PC-3 cells were significantly decreased （P <0.01）. The apoptotic rate of the PC-3 cells transfected with siRNA-ASF1B plasmid was significantly higher than that in control group （P <0.01）， and the cell cycle was arrested at G1 phase. The mRNA levels of p53， caspase-3， Bax and PARP-1 in the PC-3 cells transfected with siRNA-ASF1B plasmid were up-regulated compared with those in control group and Mack group （P <0.01）. In addition， the protein levels of MAP2K4 and p-JNK in the PC-3 cells in siRNA-ASF1B group were significantly higher than those in mock group （P <0.01）， while the protein level of p-ERK was significantly lower than that in mock group （P <0.01）. CONCLUSION ASF1B silencing induces G1 arrest and promotes apoptosis of PC-3 cells. Activating MAPK/JNK/ERK signaling pathway may be a possible contributor to the anti-prostate cancer effect of siRNA-ASF1B. 相似文献