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  • Title
  • CERTIFICATE
  • DECLARATION
  • ACKNOWLEDGEMENT
  • CONTENTS
  • ABBREVIATIONS
  • 1 Introduction and review of Literature
  • INTRODUCTION
  • Risk factors of atherosclerotic vascular disease
  • 1. Hypercholesterolaemia
  • Fig 1: Paracrine and autocrine interactions in atherosclerosis
  • 2. Triglycerides
  • 3. Lipoprotein (a)
  • 4. Blood pressure
  • 5. Epidemiological reasons
  • 6. Cigarette smoking
  • 7. Free radicals
  • Fig 2: Schematic representation for oxidative stress induced tissue injury
  • 8. Diabetes mellitus
  • 9. Coagulation system
  • 10. Platelet aggregation
  • 11. Other factors
  • a. Homocysteine and coronary risk
  • Therapy of Atherosclerotic vascular disease
  • Drugs
  • 1. Hydroxy methyl glutaryl Co A reductase inhibitors
  • 2. Bile acid binding resins
  • 3. Gemfibrozil
  • 4. Niacin
  • Animal model
  • 2 Materials and Methods
  • 2.1 MATERIALS
  • 2.1.1 Porcine Pancreas Tissue
  • 2.1.2 Plant materials
  • 2.1.3 Chemicals
  • 2.1.4 Instruments
  • 2.1.5. Animals
  • 2.1.6 Maintenance of Animals
  • 2.1.7 Test Compounds
  • 2.1.8 Preparation of test materials
  • 2.1.8a Isolation and characterisation of proteoglycans
  • Nuclease Digestion
  • Ion exchange chromatography
  • Gel filtration of proteoglycans
  • Alkali - Borohydrate digestion
  • HNO, digestion
  • Electrophoresis of HNO, digest
  • 2.1.8 b Plant extracts
  • 2.1.9 Antioxidant studies
  • 2.1.9a Superoxide radical production by photo reduction of riboflavin (204)
  • 2.1.9b Hydroxyl radical generation (205)
  • 2.1.9c Lipid peroxide formation (206)
  • 2.1.10 Lipoprotein lipase releasing activity
  • 2.1.11 Anticoagulant studies
  • 2.1.11a Plasma recalcification time
  • 2.1.11 b Activated partial thromboplastin time test
  • 2.1.12 Platelet aggregation studies (208)
  • 2.1.13 Platelet arachidonate pathway (209)
  • 2.1.14 Antiinflammatory studies
  • 2.1.15 Anti-atherogenic study
  • Aortal staining for fat deposition (214)
  • 2.1.16 Statistical evaluation
  • 3 Isolation and characterisation of proteoglycans from Porcine Pancreas
  • Introduction
  • Materials and methods
  • Results
  • Fig. 3.1: DE 52 Ion Exchange Chromato Graphy of Guanidine Extracted materials fromPorcine Pancreas
  • Fig. 3.11: Gel filtration of Proteoglycan fraction A on Sepharose 6B column
  • Fig. 3.111: Gel filtration of Proteoglycan fraction B on Sepharose 6B column
  • Fig. 3.IV: Gel filtration of Proteoglycan fraction C on Sepharose 6B column
  • Plate 3-1: Agarose gel electrophoresis of Glycosamlnoglycan moiety of PG A fraction
  • DISCUSSION
  • 4 Antioxidant and anti-inflammatory effect of some plant extracts
  • Introduction
  • Materials and methods
  • Superoxide scavenging activity
  • Hydroxyl radical scavenging activity
  • Lipid peroxide formation in vitro
  • Anti-inflammatory activity in vivo
  • Results
  • Anti-inflammatory effect of R. damascena
  • DISCUSSION
  • 5 Effect of proteoglycans and some plant extracts on lipoprotein lipase activity
  • Introduction
  • Materials and methods
  • DISCUSSION
  • 6 Antithrombotic effect of proteoglycans and some plant extracts
  • Introduction
  • Materials and methods
  • Anticoagulant activity
  • Plasma recalcification method
  • Activated prothrombin time method
  • Platelet aggregation studies in vitro
  • Study on platelet arachidonate path way in vitro
  • Anti platelet aggregatory activity
  • Effect on arachidonic acid metabolism
  • DISCUSSION
  • 7 Antiatherogenic effect of proteoglycan and acetone fraction of R.damascena
  • Introduction
  • Materials and Methods
  • Results
  • Fig. 7.I: Percentage increase in the serum lipid profile of control and treated groups compared tonormal groups one month after experiment.
  • Fig. 7. II: Percentage increase in the serum lipidprofile of control and treated groups comparedto normal groups two months after experiment.
  • Fig. 7.III: Percentage increase in the serum lipid profile of control and treated groups comparedto normal groups three months after experiment
  • Fig. 7.IV: Percentage increase in the serum lipid profile of control and treated groups comparedto normal groups four months after experiment.
  • DISCUSSION
  • Plate 7-1: Aorta of control group animals after oil red 0 stalning showing areas offat deposition
  • Plate 7-11: Aorta of AF treated group animals after oil red 0 staining showingareas of fat deposition
  • Plate 7-111: Aorta of PO A fraction treated animals after oil red 0 stdningshowlng areas of fat deposltlon
  • 8 Summary and conclusion
  • References