OBJECTIVE:To establish the quality control standard of anticancer herbal suppository METHODS:The polygonaceae and cantharidin were qualitatively and quantitatively detected by TLC and UV-spectrophotometry respectively RESU_LTS:TLC was suitable for qualitative analysis of polygonaceae and UV-spectrophotometry for quantitative analysis of cantharidin CONCLUSION:TLC and UV-spectrophotometry can be used in quality control of this preparation

Background and purpose: Pancreatic intraepithelial neoplasia (PanIN) may be a precursor lesion of inifltrating pancreatic ductal adenocarcinoma. The mutation of the phenotypic impact of K-ras G12D alone, silencing of p53 and p16 could promote this process. The role of Smad4 in this progression was poorly understood. In our previous studies, we investigated that RNA interference silence of Smad4 to promote the PanIN cell malignant transformation. In the present study, we investigate. The further explores the siRNA interference of Smad4 expression on PanIN cells could lead to proliferation and metastasis in vitro and in vivo. Methods:Smad4 knock-down PanIN cells (PanIN-S) were established by stable transfection with lentiviral-mediated Smad4 RNA interference. In vitro,silence of Smad4 enhanced the proliferation of PanIN cells as determined by cell counting. A soft agar assay was used to assess the anchorage-independent growth ability of cells. Cell migration and invasion assays were performed using transwell chambers with or without Matrigel. In xenograft model experiments, PCNA, VEGF and MMP-9 staining was separately used to evaluate cell proliferation and angiogenesis and migration (VEGF and MMP-9). Results:Effect of siRNA of Smad4 gene in PanIN cells was conifrmed by real-time RT-PCR and western blot. In vitro, silence of Smad4 enhanced the proliferation of PanIN cells as determined by cell counting. Soft agar assay showed that there were more colony cell numbers in PanIN-S cells compared with PanIN cells (P<0.05). Using the transwell assay, we observed that PanIN-S cells migrated faster than PanIN cells and similar results were obtained by Matrigel assay (P<0.05). Furthermore, immunohistochemical analysis of the harvested tumors suggested that Smad4 silencing was associated with cell proliferation (PCNA reactivity) and angiogenesis and migration (VEGF and MMP-9), and the expressions of PCNA, VEGF and MMP-9 in PanIN-S group were signiifcantly increased (P<0.05). Conclusion:Silence of Smad4 in PanIN cells enhanced progression to invasive adenocarcinoma of the pancreas by promoting cell growth, migration and invasion. Smad4 might be a new diagnostic marker in pancreatic cancer and prove to be a feasible and novel target for therapeutic intervention.

OBJECTIVE:To evaluate the pharmacodynamics and therapeutic effect of Jiakang Ⅰ oral liquid.METHODS:The drug actions of tapazole,NS and Jiakang Ⅰ were compared in the animal model of hyperthyroidism.205 hyperthyroidism cases were treated with Jiakang Ⅰ in a double blind design and the therapeutic effect was observed.RESULTS:Pharmacodynamic observation revealed that Jiakang Ⅰ could decreased T3,T4 and increase TSH significantly in rats.Compared with control group treated with tapazole or NS,in Jiakang Ⅰ group,T3 and T4 were obviously reduced and TSH was increased and the clinical symptoms were alleviated without any marked adverse reaction.CONCLUSION:The hyperthyroidism animal model can be applied to evaluating the pharmacodynamic effect of Jiakang Ⅰ.This drug has satisfactory therapeutic effect on hyperthyroidism.

Kenaf stalk was pretreated by the white-rot fungus Pleurotus sajor-caju incubated in solid-state kenaf stalk cultivation medium. Delignification and subsequent enzymatic saccharification and fermentation of kenaf stalk were investigated in order to evaluate effects of microbial pretreatment on bioconversion of kenaf lignocellulose to fuel ethanol production. The highest delignification rate of 50.20% was obtained after 25-35 days cultivation by P. sajor-caju, which could improve subsequent enzymatic hydrolysis efficiency of kenaf cellulose. And the saccharification rate of pretreated kenaf stalk reached 69.33 to 78.64%, 4.5-5.1 times higher than the control. Simultaneous saccharification and fermentation (SSF) with microbial-pretreatment kenaf stalk as substrate was performed. The highest overall ethanol yield of 68.31% with 18.35 to 18.90 mg/mL was achieved after 72 h of SSF.
Biofuels ; Ethanol ; metabolism ; Fermentation ; Hibiscus ; metabolism ; microbiology ; Lignin ; metabolism ; Plant Stems ; metabolism ; Pleurotus ; metabolism

Objective To explore the role of miR-199a-3p in osteoblast proliferation induced by fluid shear stress (FSS) and the potential molecular mechanism. Methods Osteoblast MC3T3-E1 was treated with 1. 2 Pa FSS with time gradients of 0, 15, 30, 45, 60, 75 and 90 min, respectively. MC3T3-E1 cells were transfected with miR-199a-3p mimic or miR-199a-3p inhibitor. MC3T3-E1 cells were transfected with miR-199a-3p mimic and itsnegative control and then treated with 1. 2 Pa FSS for 45 min. The pc DNA NC, pc DNA-CABLES -1, si RNA NC and si RNA CABLES-1 were transfected into MC3T3-E1 cells. The pc DNA-CABLES-1 and mir-199a-3p mimic and SI NA-cables-1 and miR-199a-3p inhibitor were co-transfected, respectively. Cell activity was detected by CCK-8 assay. Real-time quantitative PCR (RT-qPCR) was used to detect expression levels of CABLES-1, miR-199a-3p, CDK 6, Cyclin D1 and PCNA. Luciferase reporting assay was used to detect targeting relationship between CABLES-1 and miR-199a-3p. Immunofluorescence was used to detect protein expression of CABLES-1.Western blot was used to detect protein expression of CABLES-1, CDK 6, PCNA and Cyclin D1. Results Mir- 199a-3p in MC3T3-E1 cells was significantly down-regulated by FSS. Over-expressed miR-199a-3p inhibitedosteoblast proliferation, and down-regulated miR-199a-3p expression promoted osteoblast proliferation. miR-199a- 3p could reverse the FSS-induced proliferation in osteoblasts. Dual luciferase assay showed that miR-199a-3p targeted to CABLES-1 and over-expressed miR-199a-3p inhibited expression of CBALES-1 protein. CABLES-1 could promote proliferation of osteoblasts. miR-199a-3p inhibited osteoblast proliferation induced by FSS through CABLES-1. Conclusions FSS-induced osteoblast proliferation can be realized by down-regulated miR-199a-3p expression via targeting CABLES-1. The findings in this study provide new direction for researches on mechanism of FSS-induced osteoblast proliferation, as well as new ideas for future research on clinical application of mechanical loading in the treatment of bone and joint diseases.