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??OBJECTIVE To evaluate the feasibility of relay intercropping Ophiopogonis Radix and vegetables by measuring the yield and contents of effective components and fingerprint analysis. METHODS The field capacity when relay intercropping Ophiopogonis Radix and vegetables was evaluated, taking Ophiopogonis Radix monoculture as control. The contents of major compound of Ophiopogonis Radix were measured by ultraviolet spectrophotometry and high performance liquid chromatography, and the HPLC fingerprint of Ophiopogonis Radix was established. RESULTS Relay intercropping vegetables reduced the yield of Ophiopogonis Radix to some extent, but the land equivalent ratios were all more than 1, indicating that it is advantageous to intercrop Ophiopogonis Radix and vegetables.Relay intercropping vegetables did not reduce the contents of chemical constituents in Ophiopogonis Radix significantly. The similarities of all the HPLC fingerprint chromatograms were greater than 0.990. CONCLUSION Relay intercropping Ophiopogonis Radix and vegetables is a feasible pattern to solve the contention for land between Ophiopogonis Radix and vegetables in the main producing areas of Ophiopogonis Radix, and can be applied and generalized.     

HPLC同时测定麦冬中5个皂苷成分的含量

建立测定麦冬药材中麦冬皂苷D,麦冬皂苷D', ophiopojaponin C,去乙酰基ophiopojaponin A, 3-O-α-L-鼠李糖-(1→2)-β-葡萄糖麦冬苷元5种成分的HPLC方法。采用HPLC-ELSD方法,色谱柱为Kromasil 100-5C₁₈柱(4.6 mm×250 mm,5μm);流动相为乙腈(A)-水(B)溶液,梯度洗脱0~45 min,35%~55%A,体积流量1.0 mL·min^-1;柱温35℃,漂移管温度100℃,气体流速3.0 L·min^-1;进样量15μL。结果表明5种成分均达到基线分离,各成分均有较宽的线性范围和良好的线性关系(r>0.999);回收率在95.75%~103.1%。建立的麦冬皂苷含量测定方法准确灵敏、重复性好,可应用于麦冬药材质量评价中。     

Strawberry Phytochemicals Inhibit Azoxymethane/Dextran Sodium Sulfate-Induced Colorectal Carcinogenesis in Crj: CD-1 Mice

Human and experimental colon carcinogenesis are enhanced by a pro-inflammatory microenvironment. Pharmacologically driven chemopreventive agents and dietary variables are hypothesized to have future roles in the prevention of colon cancer by targeting these processes. The current study was designed to determine the ability of dietary lyophilized strawberries to inhibit inflammation-promoted colon carcinogenesis in a preclinical animal model. Mice were given a single i.p. injection of azoxymethane (10 mg kg⁻¹ body weight). One week after injection, mice were administered 2% (w/v) dextran sodium sulfate in drinking water for seven days and then an experimental diet containing chemically characterized lyophilized strawberries for the duration of the bioassay. Mice fed control diet, or experimental diet containing 2.5%, 5.0% or 10.0% strawberries displayed tumor incidence of 100%, 64%, 75% and 44%, respectively (p < 0.05). The mechanistic studies demonstrate that strawberries reduced expression of proinflammatory mediators, suppressed nitrosative stress and decreased phosphorylation of phosphatidylinositol 3-kinase, Akt, extracellular signal-regulated kinase and nuclear factor kappa B. In conclusion, strawberries target proinflammatory mediators and oncogenic signaling for the preventive efficacies against colon carcinogenesis in mice. This works supports future development of fully characterized and precisely controlled functional foods for testing in human clinical trials for this disease.     

骨髓增殖性肿瘤治疗进展:第56届美国血液学会年会报道

近年对bcr-abl阴性的骨髓增殖性肿瘤的发病机制、诊断、风险分层及治疗等方面的研究取得了长足进展,文章就2014年第56届美国血液学会(ASH)年会上关于bcr-abl阴性的骨髓增殖性肿瘤治疗进展等内容作一介绍.     

Upregulated lncRNA-UCA1 contributes to progression of hepatocellular carcinoma through inhibition of miR-216b and activation of FGFR1/ERK signaling pathway

The long non-coding RNA (lncRNA) urothelial carcinoma-associated 1 (UCA1) has been recently shown to be dysregulated, which plays an important role in the progression of several cancers. However, the biological role and clinical significance of UCA1 in the carcinogenesis of hepatocellular carcinoma (HCC) remain unclear. Herein, we found that UCA1 was aberrantly upregulated in HCC tissues and associated with TNM stage, metastasis and postoperative survival. UCA1 depletion inhibited the growth and metastasis of HCC cell lines in vitro and in vivo. Furthermore, UCA1 could act as an endogenous sponge by directly binding to miR-216b and downregulation miR-216b expression. In addition, UCA1 could reverse the inhibitory effect of miR-216b on the growth and metastasis of HCC cells, which might be involved in the derepression of fibroblast growth factor receptor 1 (FGFR1) expression, a target gene of miR-216b, and the activation of ERK signaling pathway. Taken together, our data highlights the pivotal role of UCA1 in the tumorigenesis of HCC. Moreover, the present study elucidates a novel lncRNA- miRNA-mRNA regulatory network that is UCA1-miR-216b-FGFR1-ERK signaling pathway in HCC, which may help to lead a better understanding the pathogenesis of HCC and probe the feasibility of lncRNA-directed diagnosis and therapy for this deadly disease.     

Molecular mechanisms underlying the antitumor activity of (E)-N-hydroxy-3-(1-(4-methoxyphenylsulfonyl)-1,2,3,4-tetrahydroquinolin-6-yl)acrylamide in human colorectal cancer cells in vitro and in vivo

Upregulation of class I histone deacetylases (HDAC) correlates with poor prognosis in colorectal cancer (CRC) patients. Previous study revealed that (E)-N-hydroxy-3-(1-(4-methoxyphenylsulfonyl)-1,2,3,4-tetrahydroquinolin-6-yl)acrylamide (Compound 11) is a potent and selective class I HDAC inhibitor, exhibited significant anti-proliferative activity in various human cancer cell lines. In current study, we demonstrated that compound 11 exhibited significant anti-proliferative and cytotoxic activity in CRC cells. Notably, compound 11 was less potent than SAHA in inhibiting HDAC6 as evident from the lower expression of acetyl-α-tubulin, suggesting higher selectivity for class I HDACs. Mechanistically, compound 11 induced cell-cycle arrest at the G2/M phase, activated both intrinsic- and extrinsic-apoptotic pathways, altered the expression of Bcl-2 family proteins and exerted a potent inhibitory effect on survival signals (p-Akt, p-ERK) in CRC cells. Moreover, we provide evidence that compound 11 suppressed motility, decreased mesenchymal markers (N-cadherin and vimentin) and increased epithelial marker (E-cadherin) through down-regulation of Akt. The anti-tumor activity and underlying molecular mechanisms of compound 11 were further confirmed using the HCT116 xenograft model in vivo. Our findings provide evidence of the significant anti-tumor activity of compound 11 in a preclinical model, supporting its potential as a novel therapeutic agent for CRC.