疏肝健脾解毒方对乳腺癌癌前病变肝郁证大鼠模型乳腺组织血管生成的影响

目的 研究中药疏肝健脾解毒方对乳腺癌癌前病变肝郁证大鼠模型乳腺组织微血管密度（microvessel density, MVD）、血管内皮生长因子（vascular endothelial growth factor, VEGF）及乳腺组织结构的影响,探讨其防治乳腺癌的作用机制。方法 采用二甲基苯蒽灌胃及夹尾法制备乳腺癌癌前病变肝郁证大鼠模型,随机分为模型组（蒸馏水）、中药组（疏肝健脾解毒方10.35 g/kg）、三苯氧胺组（2.0 mg/kg）,另取10只为空白对照组,分别相应干预4周后,制备乳腺组织石蜡切片进行病理学观察,采用免疫组织化学方法及Western-blot法检测各组大鼠乳腺组织中MVD及VEGF表达情况。结果 免疫组化结果显示,与模型组比较,中药组及三苯氧胺组乳腺组织非典型增生现象减少,乳腺组织MVD及VEGF水平降低,差异有统计学意义（P<0.05）,中药组MVD及VEGF水平稍低于三苯氧胺组,差异无统计学意义（P>0.05）;Western-blot结果显示：与模型组比较,中药组及三苯氧胺组乳腺组织非典型增生现象减少,乳腺组织MVD及VEGF水平降低,差异有统计学意义（P<0.05）,中药组MVD及VEGF水平与三苯氧胺组比较差异无统计学意义（P>0.05）。结论 中药疏肝健脾解毒方可在一定程度上降低乳腺癌癌前病变乳腺组织非典型增生倾向,其机制可能与降低VEGF水平、抑制新生血管生成有关。     

骨泥香辣酱的研制

为研制、生产富含钙质的骨泥香辣酱,以羊骨酶解后的骨粉为补钙原料,通过单因素和正交试验对骨粉的去膻方法、添加量及产品配方进行了研究,并分析了产品的主要质量指标。试验结果表明：骨泥香辣酱的最佳配方为鲜辣椒4JDg、辣椒酱180g、甜面酱170g、土豆泥170g、白砂糖40g;酶解后的骨粉以咖喱粉溶液去膻,在生产中,将咖喱粉配成20％的溶液,按骨粉：咖喱溶液=1：4的比例在第二次熬制时添加,骨粉添加量为最佳配方的6％：在最佳工艺条件下生产的骨泥香辣酱呈深红色,酱体表面悬浮一层红色带光泽的辣椒油,稠度适中,咸鲜微辣;香辣骨泥酱中钙的含量为116．8mgt（100g）。     

紫杉醇的研究进展

简要回顾了紫杉醇研发历史,介绍了人工栽培、半合成、全合成、真菌培养法、器官培养法、组织及细胞培养法等紫杉醇药源的研究与开发途径.阐述紫杉醇的主要剂型与国内外制剂产品的最新研究进展.展望了未来紫杉醇的发展前景.     

Phosphorus equivalency of a Citrobracter braakii phytase in broilers

A study was conducted to evaluate the effects of phytase supplementation on growth performance, phosphorus availability, and bone mineralization in broilers. Three hundred fifty Cobb × Cobb 500 slow-feathering male broilers were placed in steel battery cages into 7 treatments with 10 replications of 5 chicks each. The treatments were: a positive control (PC) diet [0.42% nonphytate phosphorus (nPP)], 4 diets containing increases in nPP from dicalcium phosphate (0.14, 0.20, 0.26, and 0.32%), and 2 phytase supplemental levels [500 and 1,000 phytase units ( FYT)/kg] on the diet having 0.14% nPP. All diets contained 0.8% calcium. Growth performance and bone data were regressed against the 4 diets having increased nPP. The equations generated were replaced by the corresponding performance obtained with 2 phytase levels to estimate their nPP bioequivalence. An overall reduction in performance and bone mineralization was observed associated with a reduction in nPP. Linear fits provided the best adjustments for all responses with the exceptions of BW gain (BWG) and feed intake (FI). Adding phytase to the 0.14% nPP diet improved growth performance and bone mineralization (P < 0.001). Average bioequivalence nPP for each phytase level was dependent on the evaluated response with lowest and highest values at 500 FYT supplementation of 0.077 and 0.145 for toe P and femur Ca, respectively, whereas lowest and highest values at 1,000 FYT of 0.143 and 0.194 for BWG and toe ash. Averaging all values for 500 and 1,000 FYT provided estimations of 0.100 and 0.166 nPP, respectively.     

蒋益兰教授治疗肝癌经验

肝癌病因病机错综复杂,尚未明确。蒋益兰教授认为脾肾亏虚乃肝癌发病之本,痰、郁、毒、痰、瘀乃致病之标。蒋益兰教授临证治疗肝癌中西医学结合,辨病辨证论治;扶正祛邪灵活运用,整体局部全面兼顾;善补气血阴阳,注重护肾保肝;未病先防,既病防变。提出健脾补肾、化瘀解毒、疏肝解郁的肝癌基本治法,临证运用,获得良好疗效。     

茶氨酸溴香酰胺对肺癌细胞生长的影响 与其作用分子机制的研究

以茶氨酸作为对照,评估现已合成的茶氨酸衍生物茶氨酸溴香酰胺(TBrC)对肺癌细胞生长的抑制作用与其分子机制.采用苔芬兰染色等方法检测不同浓度的TBrC对肺癌细胞和正常细胞生长的影响,运用Hoechst 33258荧光染色观察分析有关活性成分对肺癌细胞凋亡的诱导作用,应用蛋白质印迹法检测解析这些肺癌细胞中与凋亡和生长密切相关蛋白的表达和药物可能的作用靶点.此外,通过建立动物肿瘤模型,评价TBrC对荷瘤小鼠肺癌生长的抑制效果.实验结果显示,TBrC抑制肺癌细胞体内外生长的活性超过其母体化合物茶氨酸多倍,对正常细胞和小鼠生长无明显毒性;TBrC显示了诱导肺癌细胞凋亡的作用,其分子机制可能与抑制VEGFR1-Akt-NF-κB信号传导通路相关.本研究结果提示,TBrC具有广泛应用于临床治疗和(或)辅助治疗高转移肺癌和其他癌症的潜力.     

Biomarkers of bone development and oxidative stress in gilthead sea bream larvae fed microdiets with several levels of polar lipids and α‐tocopherol

Although dietary marine phospholipids are able to improve culture performance of marine fish larvae in a further extend than soybean lecithin, both types of phospholipids (PL) markedly increase oxidative risk. The inclusion of a fat‐soluble antioxidant such as the vitamin E α‐tocopherol could allow a better control of oxidative stress. The objective of this study was to determine the combined effect of graded levels of α‐tocopherol with different levels and sources of krill phospholipids (KPL) and soybean lecithin (SBL) on growth, survival, resistance to stress, oxidative status, bone metabolism‐related genes expression and biochemical composition of sea bream larvae. Sea bream larvae were completely weaned at 16 dph and fed for 30 days seven microdiets with three different levels of PL (0, 40 and 80 g kg^?1 diet) and two of α‐tocopherol 1500 and 3000 mg kg^?1 diet. Sea bream larvae fed diets without PL supplementation showed the lowest survival, growth and stress resistance, whereas increase in PL, particularly KPL, markedly promoted larval survival and growth. However, feeding SBL markedly increased TBARs and GPX gene expression increasing the peroxidation risk in the larvae. Besides, KPL inclusion improved incorporation of n‐3 HUFA and, particularly, EPA into larval tissues, these fatty acids being positively correlated with the expression of BMP‐4, RUNX 2, ALP, OC and OP genes and to bone mineralization for a given larval size class. The increase in dietary α‐tocopherol tends to improve growth in relation to the n‐3 HUFA levels in the diet, denoting the protective role of this vitamin against oxidation. Indeed, dietary α‐tocopherol decreased the oxidative stress in the larvae as denoted by the reduction in larval TBARs contents and gene expression of SOD and CAT, but not GPX. Thus, increase in dietary α‐tocopherol effectively prevented the formation of free radicals from HUFA, particularly EPA, but did not affect the incidence of bone anomalies or the expression of genes related to osteogenetic processes.     

Effects of HuR on cell viability,migration and invasion of gastric cancer cell line MGC-803

AIM:To investigate the effects of HuR on cell function of gastric cancer cell line MGC-803. METHODS:The mRNA expression level of HuR was detected by RT-qPCR in the tumor samples of 80 gastric cancer patients diagnosed clinically. HuR gene knock-down was achieved by transfection of si-HuR into the MGC-803 cells. The invasion, migration and viability of MGC-803 cells were measured by the scratch wound hearing, Transwell and CCK-8 assays, respectively. RESULTS:High mRNA expression of HuR was observed in 67 cases (84%) of gastric cancer tissues as compared with their control samples. Furthermore, knock-down of HuR expression effectively inhibited the invasion, migration and viability of the MGC-803 cells (P<0.05), indicating that HuR play an important role in gastric cancer as an oncogene. CONCLUSION:Abnormal expression of HuR is correlated with the progression of gastric cancer. Knock-down of HuR expression inhibits the invasion, migration and viability of MGC-803 cells.     

Effect of PDK1 on biological characteristics of lung cancer A549 cells

AIM: To investigate the effects of 3-phosphoinositide-dependent protein-1 (PDK1) on the biological characteristics of non-small-cell lung cancer cell line A549 and the underlying mechanisms.METHODS: The expression levels of PDK1 in lung normal epithelial cell line BEAS-2B and different lung cancer cell lines H460, SPCA1 and A549 were determined by Western blot and real-time PCR. Small interfering RNA was used to down-regulated PDK1 expression in the A549 cells, and then cell viability and apoptosis were measured by CCK-8 assay and flow cytometry, respectively. The expression of cell cycle-and apoptosis-related molecules at protein level and the activation of Akt/FoxO1 pathway were measured by Western blot. Insulin-like growth factor-1 (IGF-1, one of the most potent Akt activators) was used to evaluate the interaction between PDK1 and Akt/FoxO1 pathway.RESULTS: Compared with lung normal epithelial cell line BEAS-2B, PDK1 expression in the lung cancer cell lines was obviously increased (P<0.05). Knockdown of PDK1 suppressed cell viability and cell cycle, but promoted the apoptosis of the A549 cells. The results of Western blot showed that the protein levels of cyclin D1, CDK4, p-Rb, Bcl-2, p-Akt and cytoplasmic p-FoxO1 were significantly decreased after knockdown of PDK1, with increases in the protein levels of P27, cleaved caspase-3 and nuclear FoxO1. Pre-incubation with IGF-1 partly reversed the effect of PDK1 knockdown on Akt/FoxO1 pathway and increased the viability of A549 cells.CONCLUSION: In human non-small-cell lung cancer A549 cells, knockdown of PDK1 suppresses cell viability and promotes cell apoptosis by regulating the expression of cell cycle-and apoptosis-related molecules via Akt/FoxO1 pathway, suggesting that PDK1 may be a potential target for diagnosis and theatment of lung cancer.