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Hui Ma,1,2 Ping Kuen Lam,3 Wing Sum Siu,1,2 Cindy See Wai Tong,3 Kin Ki Yan Lo,3 Chi Man Koon,1,2 Xiao Xiao Wu,1,2 Xiang Li,1,2 Wen Cheng,1,2 Wai Ting Shum,1,2 Ping Chung Leung1,2 1Institute of Chinese Medicine, The Chinese University of Hong Kong, Shatin, Hong Kong, Special Administrative Region of China; 2State Key Laboratory of Research on Bioactivities and Clinical Applications of Medicinal Plants, The Chinese University of Hong Kong, Shatin, Hong Kong, Special Administrative Region of China; 3Chow Tai Fook-Cheng Yu Tung Surgical Stem Cell Research Center, Department of Surgery, The Chinese University of Hong Kong, Shatin, Hong Kong, Special Administrative Region of ChinaCorrespondence: Ping Chung LeungInstitute of Chinese Medicine, The Chinese University of Hong Kong, Shatin, Hong Kong, Special Administrative Region of ChinaTel +85222528868Email pingcleung@cuhk.edu.hkIntroduction: The biological role of mesenchymal stem cells (MSCs) in wound healing has been demonstrated. However, there were limited studies on the healing effect of secretome which consists of many biological factors secreted by MSCs. In this study, we aimed to compare the therapeutic effects of secretome with MSCs on facilitating wound healing.Methods: Green fluorescent protein labelled adipose-derived MSCs (GFP-ADMSCs) or secretome was injected in the full-thickness skin excision model on SD rats. The wound healing process was evaluated by calculating the healing rate and the histological examinations on skin biopsy. The cell viability, proliferation and mobility of the rat dermal fibroblasts were compared after different treatments. The inflammatory response in macrophages was indicated by the level of nitric oxide (NO) and inflammatory cytokines through NO assay and ELISA.Results: On day 5 and day 14, both MSCs and secretome accelerated the wound healing, secretome further enhanced the process. GFP-MSCs were detected 10 days after transplantation. The level of IL-6 and TNF-α in blood was re

Aim of the study: A novel topical paste used for fracture healing (FH), consisting of the extracts of six herbs, Radix Dipsaci, Ramulus Sambucus Williamsu. Rhizoma Notoginseng, Flos Carthami, Rhizoma Rhei and Fructus Gardeniae, was developed according to the classical theory of traditional Chinese medicine This study aimed to determine the effectiveness of this formula, and some of its important chemical components in the promotion of fracture healing. The transdermal transport of FH was also examined. Materials and methods The osteogenic, angiogenic and nitric oxide suppressing effects of FH and its Important chemical marker components were assessed by using osteoblastosacroma UMR-106 cells, human umbilical vein endothelial cells (HUVEC) and murine macrophage RAW264 7 cells, respectively. The bone healing effects of the FH paste and its transdermal absorption were determined using a rabbit fracture model. The callus sizes, bone specific alkaline phosphatase levels and biomechanical properties of the healed bone were assessed. Results FH significantly increased the cell proliferation in UMR-106 and HUVEC cells and inhibited the nitric oxide production in murine macrophage in dose-dependent manner. Its important chemical components asperosaponin VI, ginsenoside Rg1 and emodin were shown to be acting positively in the respective in vitro studies FH paste significantly improved the bone healing in the rabbit fracture model, as was indicated by the Increases in callus size at weeks 2-5, and the elevations in bone specific alkaline phosphatase activities at weeks 5-6. The analysis using LC/MS/MS also showed the presence of important chemical marker components of the FH formula in the plasma after 8 weeks of topical treatment. Conclusion: This study presents the first scientific evidence of the efficacy of a herbal paste in the promotion of fracture healing. There were evidences of transdermal transport of the chemical components, control the inflammation through nitric o

Atherosclerosis is the chief cause of acute coronary syndromes and may progress for many years before any noticeable clinical syndromes occur. Hyperlipidemia is the common clinical problem for people adopting a western style of living and it can initiate a series of vascular events that result in atherosclerosis. The pathological processes include the accumulation of modified lipid, mainly oxidized low-density lipoprotein (oxLDL), endothelial cell dysfunction and activation, increase in expression of adhesion molecules, activation and recruitment of inflammatory cells and induction of proliferation and migration of vascular smooth muscle cells., Endothelial-monocyte adhesion is crucial process for the recruitment of monocyte into intima. DG (7:3), Danshen and SAB were found to inhibit TNF-alpha-induced endothelial-monocyte adhesion. They also showed inhibition on TNF-alpha induced production of chemokines, MCP-1 which promotes the transmigration of monocyte. However, it did not inhibit the production of cytokine, IL-6 which stimulates the expression of adhesion molecules such as VCAM-1 and ICAM-1., For the in vivo study, DG (7:3) exhibited no anti-hyperlipidemic or hypolipidemic effect against diet-induced hyperlipidemia, nor did it lower cholesterol level in hamsters. Also, it did not inhibit HMG-CoA reductase activity or increase the total fecal sterols excretion. However, DG (7:3) exhibited hypocholesterolemic effect on diet-induced hyperlipidemia in the rabbit model, wherein it could lower plasma total cholesterol and liver cholesterol level. Moreover, it could significantly decrease the atheroma formation., In the present study, the anti-oxidative effects of herbal extract/compound were measured by three in vitro assays, namely the inhibition of 2,2'-azobis(2-amidinopropane)dihydrochloride (AAPH)-induced red blood cells hemolysis, AAPH-induced cardiomyocyte (H9c2) cells death and Cu2+-induced low-density lipoprotein oxidation. The results showed that the aqueous extract of the compound formula Danshen (D) and Gegen (G) (7:3), abbreviated as DG (7:3), and an aqueous extract of Danshen as well as salvianolic acid B (SAB) exhibited anti-oxidant effect, but Gegen did not produce such effect. It was found that SAB showed a stronger anti-oxidant effect than that of ascorbic acid., Proliferation and migration of vascular smooth muscle cells (vSMCs) are important pathological processes involved in the development of atherosclerosis. DG (7:3), Danshen and SAB were found to inhibit PDGF-induced vSMCs proliferation through G1/S cell cycle arrest. Cyclin D, a main component that governs the transition of G1 phase to S phase, was found to be down-regulated by DG (7:3), Danshen and SAB, as assessed by measurements of both protein and mRNA levels. Moreover, DG (7:3), Danshen and SAB showed anti-migratory effect against platelet-derived growth factor-induced vSMCs migration., To summarize, DG (7:3) was found to have potential to produce anti-atherosclerotic effect by inhibiting the LDL oxidation, proliferation and migration of vascular SMC, thereby preventing the formation of atheroma plaque., Koon Chi Man., "March 2006.", Adviser: Kwok Pui Fung., Source: Dissertation Abstracts International, Volume: 67-11, Section: B, page: 6324., Thesis (Ph.D.)--Chinese University of Hong Kong, 2006., Includes bibliographical references (p. 246-264)., Electronic reproduction. Hong Kong : Chinese University of Hong Kong, [2012] System requirements: Adobe Acrobat Reader. Available via World Wide Web., Electronic reproduction. [Ann Arbor, MI] : ProQuest Information and Learning, [200-] System requirements: Adobe Acrobat Reader. Available via World Wide Web., s in English and Chinese., School code: 1307., isbn: 9780542966040, Use of this resource is governed by the terms and conditions of the Creative Commons “Attribution-NonCommercial-NoDerivatives 4.0 International” License (http://creativecommons.org/licenses/by-nc-nd/4.0/)

Koon Chi Man., Thesis (M.Phil.)--Chinese University of Hong Kong, 2000., Includes bibliographical references (leaves 158-174)., s in English and Chinese., Acknowledgment --- p.i, Abbreviations --- p.ii, p.v, Chinese Abstract --- p.viii, Table of Content --- p.x, Chapter Chapter one: --- Introduction --- p.1, Chapter 1.1 --- Introduction --- p.1, Chapter 1.2 --- Classification of Plant Polysaccharides --- p.2, Chapter 1.2.1 --- Definition of Dietary Fiber --- p.3, Chapter 1.2.2 --- Types of Soluble Dietary Fiber --- p.3, Chapter 1.3 --- Physiological Effect of Fiber --- p.6, Chapter 1.3.1 --- Reduction in Absorption by Viscous Polysaccharides --- p.7, Chapter 1.3.2 --- Gastric Emptying --- p.7, Chapter 1.3.3 --- Effect of Viscous Polysaccharides on Intraluminal Mixing --- p.8, Chapter 1.3.4 --- Effect of Luminal Secretions on Viscosity --- p.9, Chapter 1.4 --- Physicochemical Qualities and Hypocholesterolemic Effects --- p.9, Chapter 1.5 --- Gastrointestinal Events and Hypocholesterolemic Effects --- p.11, Chapter 1.5.1 --- Mouth --- p.11, Chapter 1.5.2 --- Stomach --- p.12, Chapter 1.5.3 --- Small intestine --- p.12, Chapter 1.5.4 --- Large intestine --- p.13, Chapter 1.6 --- Proposed Mechanisms for Hypocholesterolemic Effects --- p.13, Chapter 1.6.1 --- Altered Bile Acid Absorption and Metabolism --- p.14, Chapter 1.6.2 --- Modified Lipid Absorption and Metabolism --- p.15, Chapter 1.6.3 --- Effects of SCFA on Lipid Metabolism --- p.15, Chapter 1.6.4 --- Changed Hormone Concentrations --- p.16, Chapter Chapter Two: --- Materials and Methods --- p.17, Chapter 2.1 --- Materials --- p.17, Chapter 2.1.1 --- Fungus --- p.17, Chapter 2.1.2 --- Animals --- p.17, Chapter 2.1.2.1 --- Golden Syrian Hamster --- p.17, Chapter 2.1.2.2 --- Rabbit --- p.18, Chapter 2.1.3 --- Characterization of Auricularia Polytricha --- p.18, Chapter 2.1.4 --- Chromatographic materials --- p.22, Chapter 2.1.5 --- "Determination of Plasma TC，HDL-C, LDL-C，TG，AST and ALT" --- p.24, Chapter 2.1.6 --- HMG-CoA Reductase Activity Assay --- p.26, Chapter 2.1.7 --- "Quantitative Determination of Liver Cholesterol, Acidic and Neutral Sterol" --- p.27, Chapter 2.1.8 --- Animal Diets --- p.29, Chapter 2.1.8.1 --- Hamster Diets --- p.29, Chapter 2.1.8.2 --- Rabbit Diets --- p.29, Chapter 2.2 --- Methods --- p.33, Chapter 2.2.1. --- Extraction of Water-Soluble AP Polysaccharide (APP) --- p.33, Chapter 2.2.2. --- Characterization of Auricularia Polytricha --- p.34, Chapter 2.2.2.1 --- Determination of carbohydrate content of AP Polysaccharide --- p.34, Chapter 2.2.2.2 --- Determination of uronic acid content of AP Polysaccharide --- p.34, Chapter 2.2.2.3 --- Determination of protein content of AP Polysaccharide by BCA protein assay --- p.35, Chapter 2.2.2.4 --- Determination of component sugar units of AP Polysaccharide --- p.35, Chapter 2.2.2.5 --- Fractionation of AP Polysaccharide --- p.36, Chapter 2.2.2.6 --- Determination of monosaccharides of AP Polysaccharide by HPLC --- p.37, Chapter 2.2.3 --- "Determination of plasma TC, HDL-C, LDL-C,TG,AST and ALT" --- p.39, Chapter 2.2.3.1 --- Plasma Total Cholesterol --- p.39, Chapter 2.2.3.2 --- Plasma HDL-Cholesterol --- p.40, Chapter 2.2.3.3 --- Plasma LDL-Cholesterol --- p.40, Chapter 2.2.3.4 --- Plasma Triglyceride --- p.41, Chapter 2.2.3.5 --- Plasma Aspartate Aminotransferase --- p.41, Chapter 2.2.3.6 --- Plasma Alanine Aminotransferase --- p.42, Chapter 2.2.4 --- HMG-CoA Reductase Activity Assay --- p.42, Chapter 2.2.4.1 --- Preparation of Hepatic Microsome --- p.42, Chapter 2.2.4.2 --- HMG-CoA Activity Assay --- p.43, Chapter 2.2.5 --- Quantitative Determination of Liver Cholesterol --- p.44, Chapter 2.2.5.1 --- Cholesterol Extraction and its Silylation --- p.44, Chapter 2.2.5.2 --- GLC Analysis of TMS-Ether Derivative of Cholesterol --- p.45, Chapter 2.2.6 --- Quantitative Determination of Neutral and Acidic Sterols --- p.45, Chapter 2.2.6.1 --- Separation of Neutral and Acidic Sterols --- p.45, Chapter 2.2.6.2 --- Conversion of Neutral Sterols to its TMS-Ether Derivative --- p.46, Chapter 2.2.6.3 --- Conversion of Acidic Sterols to its TMS-Ether Derivatives --- p.46, Chapter 2.2.6.4 --- GLC Analysis of Neutral and Acidic Sterols --- p.47, Chapter 2.2.7 --- Study of Atherosclerosis of Rabbit --- p.48, Chapter 2.2.7.1 --- Sudan III staining of the thoracic aorta --- p.48, Chapter 2.2.7.2 --- Measurement of atheroma formation in the aorta --- p.49, Chapter 2.2.8 --- Animal Experiments --- p.51, Chapter 2.2.8.1 --- Protective Effect of APP in Hyperlipidemic Study (Exp. 1) --- p.51, Chapter 2.2.8.2 --- Therapeutic Effect of APP in Hyperlipidemic Study (Exp. 2) --- p.52, Chapter 2.2.8.3 --- Dose Response of APP in Hyperlipidemic Study (Exp. 3) --- p.52, Chapter 2.2.8.4 --- Hypolipidemic Effect of Short Chain Fatty Acid (Exp. 4) --- p.53, Chapter 2.2.8.5 --- Effect of APP and SCFA on HMG-CoA Reductase Activity (Exp5） --- p.53, Chapter 2.2.8.6 --- Hypolipidemic and Anti-atherosclerotic Effect of APP (Exp. 6) ´Ø… --- p.54, Chapter 2.3 --- Statistical analysis --- p.54, Chapter Chapter Three: --- Fractionation and Characterization of Auricularia Polytricha Polysaccharide --- p.55, Chapter 3.1 --- Introduction --- p.55, Chapter 3.2 --- Fungal polysaccharides from Auricularia Polytricha --- p.55, Chapter 3.3 --- Results --- p.57, Chapter 3.3.1 --- Extraction and Fractionation of Auricularia Polytricha --- p.57, Chapter 3.3.2 --- Determination of Carbohydrates Content --- p.58, Chapter 3.3.3 --- Determination of Protein Content --- p.61, Chapter 3.3.4 --- Determination of Uronic Acid Content --- p.61, Chapter 3.3.5 --- Determination of component sugars of AP Polysaccharide --- p.65, Chapter 3.3.6 --- Fractionation of AP Polysaccharide --- p.67, Chapter 3.3.7 --- Determination of monosaccharide components of AP Polysaccharide by HPLC --- p.72, Chapter 3.4 --- Discussion --- p.79, Chapter Chapter Four: --- "Protective, Therapeutic and Dose Effect of Auricularia Polytricha Polysaccharide (APP) on Hyperlipidemia" --- p.83, Chapter 4.1 --- Introduction --- p.83, Chapter 4.2 --- Results (Exp. 1) --- p.86, Chapter 4.2.1 --- Body Weight and Food Intake --- p.86, Chapter 4.2.2 --- Effect of APP Supplementation on Hepatic Cholesterol --- p.86, Chapter 4.2.3 --- "Effect of APP Supplementation on Plasma TC, HDL-C and TG" --- p.87, Chapter 4.2.4 --- Effect of APP Supplementation on Fecal Output of Neutral Sterols --- p.94, Chapter 4.2.5 --- Effect of APP Supplementation on Fecal Output of Acidic Sterols --- p.94, Chapter 4.3 --- Discussion (Exp. 1) --- p.99, Chapter 4.4 --- Results (Exp. 2) --- p.102, Chapter 4.4.1 --- Body Weight and Food Intake --- p.102, Chapter 4.4.2 --- Effect of APP Supplementation on Hepatic Cholesterol --- p.102, Chapter 4.4.3 --- Effect of APP Supplementation on Plasma TC and TG --- p.103, Chapter 4.4.4 --- Effect of APP Supplementation on Plasma HDL-C and LDL-C --- p.104, Chapter 4.5 --- Discussion (Exp. 2) --- p.109, Chapter 4.6 --- Results (Exp. 3) --- p.111, Chapter 4.6.1 --- Body Weight and Food Intake --- p.111, Chapter 4.6.2 --- Dose Response of APP Supplementation on Hepatic Cholesterol --- p.111, Chapter 4.6.3 --- Dose Response of APP Supplementation on Plasma TG --- p.112, Chapter 4.6.4 --- Dose Response of APP Supplementation on Plasma HDL-C and LDL-C --- p.112, Chapter 4.6.5 --- Dose Response of APP Supplementation on ALT and AST Activity --- p.113, Chapter 4.6.6 --- Dose Response of APP Supplementation on Fecal Output of Neutral and Acidic Sterols --- p.113, Chapter 4.7 --- Discussion --- p.121, Chapter Chapter Five: --- Hypolipidemic Effect of Short Chain Fatty Acids --- p.123, Chapter 5.1 --- "Introduction (Exp. 4,5)" --- p.123, Chapter 5.2 --- "Results (Exp. 4,5)" --- p.125, Chapter 5.2.1 --- Body Weight and Food Intake --- p.125, Chapter 5.2.2 --- Effect of SCFA Supplementation on Hepatic Cholesterol --- p.125, Chapter 5.2.3 --- "Effect of SCFA Supplementation on Plasma TG, HDL-C and LDL-C" --- p.128, Chapter 5.2.4 --- Effect of SCFA Supplementation on AST and ALT Activity --- p.128, Chapter 5.2.5 --- Effect of SCFA supplementation on HMG-CoA Reductase Activity --- p.133, Chapter 5.3 --- "Discussion (Exp. 4,5)" --- p.135, Chapter Chapter Six: --- Hypolipidemic and Antiatherosclerotic Effect of APP --- p.137, Chapter 6.1 --- Introduction (Exp. 6) --- p.137, Chapter 6.2 --- Results (Exp. 6) --- p.139, Chapter 6.2.1 --- Body Weight and Food Intake --- p.139, Chapter 6.2.2 --- Effect of APP Supplementation on Hepatic Cholesterol --- p.139, Chapter 6.2.3 --- "Effect of APP Supplementation on Plasma TG, HDL- and LDL-C" --- p.141, Chapter 6.2.3 --- Effect of APP Supplementation on AST and ALT Activity --- p.142, Chapter 6.2.5 --- Effect of APP supplementation on HMG-CoA Reductase Activity --- p.146, Chapter 6.2.6 --- Effect of APP supplementation on the Formation of Atheroma --- p.146, Chapter 6.3 --- Discussion (Exp. 6) --- p.151, Chapter Chapter Seven: --- General Discussion and Future Perspectives --- p.153, References --- p.158, http://library.cuhk.edu.hk/record=b5895813, Use of this resource is governed by the terms and conditions of the Creative Commons “Attribution-NonCommercial-NoDerivatives 4.0 International” License (http://creativecommons.org/licenses/by-nc-nd/4.0/)