Ingredient co brandi的問題，透過圖書和論文來找解法和答案更準確安心。 我們找到下列包括價格和評價等資訊懶人包

Identification of active agents inducing ossification and novel biomarkers associated with osteoporosis

為了解決Ingredient co brandi的問題，作者Zuha Imtiyaz 這樣論述：

TABLE OF CONTENTSABSTRACT ixLIST OF ABBREVIATIONS xi1. INTRODUCTION 11.1 Bone and bone remodeling 11.2 Osteoporosis 61.2.1 Disease epidemiology 71.2.2 Current drugs used for osteoporosis and their mode of action 91.3 Biomarkers of bone formation 121.3.1 SNPs as biomarkers 161.4 Relation of

FTCDNL1 gene with osteoporosis 191.5 Herbs with medicinal value for bone formation 20RATIONALE 25AIM 262. MATERIALS AND METHODS 272.1 Reagents and chemicals used 272.2 Extraction and isolation 292.2.1 Turpinia formosana Nakai. 292.2.2 Euonymus spraguei Hayata. 292.3 Cell culture 302.3.1 H

uman osteoblast (HOb) cells 302.3.2 Human osteosarcoma (MG-63) cells 302.3.3 Cell culture of RAW 264.7 cells and differentiated osteoclasts 312.4 MTT assay for cell viability assay 312.5 ALP activity assay 312.6 Mineralization assay 322.7 RNA isolation and reverse transcription 322.8 Real-tim

e quantitative PCR analysis 332.9 Estrogen receptor expression assay 352.10 Plasmid DNA purification 352.11 DNA transfection 362.12 siRNA transfection 362.13 Western blot 372.14 Immunofluorescence 372.15 Statistical Analysis 383. RESULTS 393.1 Elucidating osteogenic potential of compounds i

solated from Turpinia formosana Nakai 393.1.1 Isolated compounds from Turpinia formosana 393.1.2. Cytotoxicity of compounds isolated from T. formosana in HOb cells 413.1.3 Effect of isolated compounds on ALP activity in HOb cells 433.1.4 Effect of isolated compounds on mineralization in HOb cell

s 453.1.5 Effect of isolated compounds on estrogen receptor expression in HOb cells 473.1.6 Effect of isolated compounds on the genetic markers of bone formation in HOb cells 493.2. Isolated compounds from Euonymus spraguei mediate of osteogenesis through multiple pathways 523.2.1 Effect of vari

ous extractants for E. spraguei on cell viability, ALP activity and mineralization in HOb cells 523.2.2 Compounds isolated from ES 563.2.3 Effect of syringin (8) and (-)-epicatechin (9) on the viability of HOb cells 573.2.4 Effect of syrngin (8) and (-)-epicatechin (9) on ALP activity in HOb cell

s 583.2.5 Effect of syrngin (8) and (-)-epicatechin (9) on mineralization in HOb cells 603.2.6 Effect of syrngin (8) and (-)-epicatechin (9) on Estrogen receptor (ER) expression 623.2.7 Effect of syringin (8) and (-)-epicatechin (9) on the mRNA expression levels of bone remodelling-related genes

633.2.8 Effect of syringin (8) and (-)-epicatechin (9) on BMP-2 pathway 663.2.9 Effect of syringin (8) and (-)-epicatechin (9) on RANKL/OPG 693.2.10 Effect of syringin (8) and (-)-epicatechin (9) on autophagy 713.2.11 Effect of syringin (8) and (-)-epicatechin (9) on OPN expression 733.2.12 Eff

ect of syringin (8) and (-)-epicatechin (9) on the viability of RANKL-induced osteoclasts 753.3. Elucidating the association between FTCDNL1 on bone formation and its role in osteoporosis onset 773.3.1 Transfection of FTCDNL1 into MG-63 cells 773.3.2 Effect of FCTDNL1 overexpression on bone forma

tion-related genes 793.3.3 Effect of FTCDNL1 knockdown on cell viability of MG63 cells 833.3.4 Effect of FTCDNL1 knockdown on ALP activity in MG63 cells 844. DISCUSSION 854.1. Elucidating osteogenic potential of compounds isolated from Turpinia formosana 874.2 Isolated compounds from Euonymus

spraguei mediate of osteogenesis through multiple pathways 904.3. Elucidating the association between FTCDNL1 on bone formation and its role in osteoporosis onset 945. CONCLUSION 96LIST OF PUBLICATIONS 97BIBLIOGRAPHY 98 LIST OF FIGURESFig 1. Types of cells found within the bone tissue 1Fig 2.

Interplay between osteoblasts and osteoclasts 3Fig 3. Involvement of various cells at different stages of bone remodelling 4Fig 4. Static and dynamic changes in bone 7Fig 5. Growth rate of osteoporosis, estimated number of osteoporotic fracture worldwide by 2050 9Fig 6. Mechanism of action of th

e current drugs for osteoporosis. 11Fig 7. Role of various biomarkers at various stages of bone formation 14Fig 8. Signalling cascade of BMP-2 pathway. 16Fig 9. Display of the importance of a SNP and its significance in the phenotype 17Fig 10. Pictorial representation of aim of the study. 26Fig

11. Structures of the isolated compounds elucidated using various spectroscopic techniques. 40Fig 12. Cytotoxic effect of compounds isolated from T.formosna. 41Fig 13. Induction of ALP activity by 1, 2, 3 and 6. 43Fig 14. Mineral deposition by 1, 2, 3 and 6. 46Fig 15. Expression of ERs affected

by 1, 2, 3, and 6. 48Fig 16. 1 elevates mRNA expression of bone formation-related genes. 50Fig 17. Pictorial summary of underlying mechanism for osteogenesis by 1. 51Fig 18. Solvent test for extraction of E. spraguei (ES). 54Fig 19. Structure of compounds isolated from ES. 56Fig 20. Cell viabi

lity of HOb cells on 8 and 9 treatments. 57Fig 21. Induction of ALP activity by 8 and 9. 58Fig 22. Mineral deposition by 8 and 9.. 61Fig 23. Influence of 8 and 9 on ER expression. 62Fig 24. Expression of bone formation-related genes after 8 and 9 treatments.. 65Fig 25. 8 and 9 mediates their ef

fect via BMP-2 signalling pathway. 67Fig 26. Attenuation of RANKL/OPG ratio by 8 and 9. 69Fig 27. Modulation of autophagy by 8 and 9. 72Fig 28. Induction of OPN by 8 and 9. 74Fig 29. Cytotoxic effect of 8 and 9 on osteoclasts. 75Fig 30. Pictorial summary of osteogenesis induced by 8 and 9. 76F

ig 31. Transient transfection of FCTDNL1 in MG63 cells. 78Fig 32. mRNA expression levels of bone formation related biomarkers after FTCDNL1 overexpression. 81Fig 33. FTCDNL1 knockdown does not affect viability of MG63 cells. 83Fig 34. ALP activity of MG63 cells after FTCDNL1 knockdown. 84Fig 35.

Mechanism of 8 and 9 in RANK-RANKL interaction 92Fig 36. Role of autophagy in bone formation. 93Fig 37. Pictorial representation of osteogenesis with FTCDNL1 and future prospects. 95LIST OF TABLESTable 1. Primer and probe combination used for real-time PCR 34Table 2. Primer sequences used for r

eal-time PCR 35Table 3. Sequences of siRNA used for FTCDNL1 knockdown 37Table 4. Phytochemical as therapeutic agents and their plant source 85

大蒜有機硫化合物diallylsulfide與diallyldisulfide對血管新生作用及其相關因子之影響

為了解決Ingredient co brandi的問題，作者周歆倩 這樣論述：

本研究為利用細胞及動物模式探討大蒜有機硫化合物對血管新生作用及其相關因子之影響。細胞實驗方面，分別在有無10 ng/ml VEGF投予下，給予血管內皮EA hy 926細胞DAS (diallyl sulfide) 及DADS (diallyl disulfide) 後，分析有機硫化合物對細胞生長及血管新生相關因子之影響。結果顯示，大蒜萃取物DAS (2.5~7.5 μM) 及DADS (0.05~0.5 μM) 可抑制EA hy 926細胞之生長與增生，但可促進血管新生過程最後階段-類血管 (tube formation) 之生成，且此影響與促血管新生因子VEGF、IL-8及活化型MMP-

2表現增加相關。在VEGF誘導血管新生下，DAS、DADS及二者合併使用皆可抑制因VEGF誘導之EA hy 926細胞增生及類血管生成，其影響與增加IL-8及降低活化型MMP-2表現相關。於動物實驗方面，以皮下注射含有無1 μg/ml bFGF (basic fibroblast growth factor) 之matrigel，以誘導C57BL/6小鼠病理性血管新生作用後，結果顯示，連續10天腹腔注射DAS (12.5 mg/kg)、DADS (50 mg/kg) 及合併使用組別，matrigel中之血紅素含量有低於bFGF組之傾向，但無顯著差異。總而言之，大蒜可促進細胞生理性血管新生，且抑

制VEGF誘導之細胞血管新生作用，其作用與調節血管新生相關因子VEGF、IL-8及MMP-2表現相關，但動物實驗結果有待進一步確認之。關鍵字: 大蒜有機硫化合物、血管新生、癌症、傷口癒合