Phytochemical and anti-inflammatory properties of methanol extract of crateva adansonii stem bark.

 

Table Of Contents


Chapter ONE

INTRODUCTION

  • 1.1Introduction
  • 1.2Background of Study
  • 1.3Problem Statement
  • 1.4Objective of Study
  • 1.5Limitation of Study
  • 1.6Scope of Study
  • 1.7Significance of Study
  • 1.8Structure of the Research
  • 1.9Definition of Terms

Chapter TWO

LITERATURE REVIEW

  • 2.1Overview of Phytochemicals
  • 2.2Phytochemical Composition of Crateva Adansonii
  • 2.3Anti-inflammatory Properties of Plants
  • 2.4Literature Review on Methanol Extraction
  • 2.5Previous Studies on Crateva Adansonii
  • 2.6Mechanisms of Anti-inflammatory Action
  • 2.7Effects of Phytochemicals on Inflammation
  • 2.8Role of Stem Bark Extracts in Traditional Medicine
  • 2.9Comparative Analysis of Anti-inflammatory Agents
  • 2.10Importance of Studying Phytochemicals

Chapter THREE

RESEARCH METHODOLOGY

  • 3.1Research Methodology Overview
  • 3.2Selection of Research Design
  • 3.3Sampling Techniques
  • 3.4Data Collection Methods
  • 3.5Data Analysis Procedures
  • 3.6Experimental Setup and Procedures
  • 3.7Ethical Considerations
  • 3.8Validity and Reliability Assurance

Chapter FOUR

DATA PRESENTATION AND ANALYSIS

  • 4.1Data Presentation and Analysis
  • 4.2Phytochemical Analysis Results
  • 4.3Anti-inflammatory Effects Data
  • 4.4Comparison with Existing Literature
  • 4.5Interpretation of Findings
  • 4.6Discussion on Methodological Choices
  • 4.7Implications of Results
  • 4.8Recommendations for Future Research

Chapter FIVE

SUMMARY, CONCLUSION AND RECOMMENDATIONS

  • 5.1Summary of Findings
  • 5.2Conclusion
  • 5.3Contributions to Knowledge
  • 5.4Practical Implications
  • 5.5Limitations of the Study
  • 5.6Suggestions for Further Research

Project Abstract

<p> This research investigated the phytochemical and anti-inflammatory<br>properties of methanol extract of Crateva adansonii stem bark. Although<br>several edible and non-edible plants parts are used in inflammatory<br>treatment, many record has been found of the use of Crateva adansonii<br>stem bark. For this research, fresh stem bark of Crateva adansonii were<br>collected from Asata village in Enugu State. The cuttings were authenticated<br>at the Bioresource development centre. They were then dried at room<br>temperature for one month in an open lab space, grounded into powder and<br>weighed on a beam balance as 460.6g. The powder was soaked for twentyfour<br>to fourty-eight hours in methanol to get a methanol extract and then<br>concentrated into paste at a set temperature range of 30-550C in a water<br>bath. A population of twenty adult wistar Albino rats was used for antiinflammatory<br>test. The rats were divided into five (5) groups of four (4)<br>albino rats each. They were administered 3% tween-80 mixed with<br>dichloromethane extract of Crateva adansonii and the control was<br>administered with 0.5ml of 3% tween-80. Acute inflammation was induced<br>an hour after test substances were administered by injecting egg albumin in<br>the subplanter region of the right hind paw and edema assessed by mercury<br>displacement for a period of 0-180 minutes. Anti-inflammatory effect was<br>significant within 30 minutes of induced edema with inhibition occurring in<br>three phases of 0-30, 30-60, 60-90. 90-120 to 180 minutes. Inhibition was<br>highest at the third phase. Crateva adansonii barks showed antiinflammatory<br>effect by inhibiting β€œprostaglandin” synthesis an inflammatory<br>mediator. <br></p>

Project Overview

<p> 1.0 INTRODUCTION<br>Inflation is a Latin word (inflammare) which is translated means to set on<br>fire. It is a complex biological response of vascular tissue to harmful stimuli<br>such as pathogens, damaged cells irritant. Inflammation is the reaction of<br>vascularized tissue to local injury caused by certain stimuli like infections,<br>chemicals and biochemical agents, thermal or other physical trauma,<br>antigen-antibody interaction etc (Carol, 1994). Without inflammatory<br>response, wounds will not heal and minor infections would be over weening.<br>Though inflammation aims at limiting damage and restoring function, some<br>enzymes and toxic products within phagocytic cells are released to the<br>extend of damaging the tissue. The advent of anti-inflammatory agents has<br>made inflammation which as been a threat to human life due to its complex,<br>multicontent, to loose its power. These anti-inflammatory agents or drugs<br>help reduce, pain by inhibiting inflammation as opposed to opioids, which<br>affects the central nervous system. It also prevent repairs, prevent and stop<br>the consequences of inflammation by acting on the body responses without<br>directly antagonizing the causative agent (Stedman, 2000). These antiinflammatory<br>process involves the process of balancing pro-inflammatory<br>acute-phase reactants (Russell et al. 2000), altering biochemical pathway<br>78<br>forming prostaglandins by inhibiting cyclooxygenase enzyme from<br>catalyzing the reaction, as a result, suppress, compensate and correct the<br>mechanical and structural abnormalities by assistive device. (Masumoto et<br>al.2009).<br>The inflammatory reaction is phylogenetically and ontogenetically the oldest<br>defense mechanism. The cells of immune system are widely distributed<br>throughout the body, but if an infection or tissue damage occurs. It is<br>necessary to concentrate them and their products at the site of damage.<br>Three major events occurring during this response:<br>1. An increased blood supply to the damaged tissue . It is performed by<br>vasodilation. The inflamed tissue look like containing greater number<br>of vessels.<br>2. Increased capillary permeability caused by retraction of the<br>endothelial cells. This permits larger molecules than usual to escape<br>from the capillaries, and thus allows the soluble mediators of<br>immunity to reach the site of inflammation.<br>3. Leukocytes migrates out of the capillaries into the surrounding tissues.<br>In the earliest stages of inflammation, neutrophils are particularly<br>78<br>prevalent, but later monocytes and lymphocytes migrate towards the<br>site of infection (Ashcroft et al.1999).<br>For the possibility of surrounding tissue damage, inflammatory responses<br>must be well ordered and controlled. The body must be able to act quickly in<br>some situations, for example to reduce or stop the lost of blood, whereas<br>tissue repair can begin later. Therefore a wide variety of interconnected<br>cellular and humoral (soluble) mechanisms are activated when tissue<br>damage and infections occur. On the other hand, if injury is negligible, the<br>body must have mechanisms which are able to stop tissue damage when the<br>agent is removed. The development of inflammatory reactions is controlled<br>by cytokines, products of plasma enzymes (complement, the coagulation<br>clotting, kinin and fibrolytic pathways), by lipid mediators (prostaglandin<br>and leukotrienes) released from different cells/ and by vasoactive mediators<br>from the mast cells, basophils and platelets. These anti-inflammatory<br>reactions differ. Fast-acting mediators such as vasoactive amines and the<br>product of the kininsystem, modulate the immediate response. Later, newly<br>synthesized mediators such as leukotrienes are involved in the accumulation<br>and activation of other cells. However, in inflammatory reactions initiated<br>by the immune system, the ultimate control is exerted by the antigen itself in<br>the same ways it controls the immune response itself. For this reason, the<br>78<br>cellular accumulation at the site of chronic infection or auto-immune<br>reactions where antigen cannot ultimately be eradicated, is quiet different<br>from the sites were antigenic stimulus can be rapidly cleared.<br>The nervous system can also participate in the control of inflammation<br>especially axon reflexes, but inflammation may be realized in non-nervous<br>tissues as well.<br>Inflammation may become chronic in certain settings where the acute<br>process characterized by neutrophil infiltration and swelling gives way to<br>predominance of mononuclear phagocytes and lymphocytes.This probably<br>occurs to some degree with the normal healing process but becomes<br>exaggerated and chronic when there’s ineffective elimination of foreign<br>materials as in certain infections (e.g tuberculosis) or following introduction<br>of foreign bodies (example asbestos) or deposition of crystals (example urate<br>crystals). Chronic inflammation is often associated with fussion of<br>mononuclear cells to form multinucleated gigantic cells, which eventually<br>become granuloma. Chronic inflammation is seen under of delayed<br>hypersensitivity (Nathan, 2002).<br>78<br>1.2 CRATEVA ADANSONII AS A PLANT.<br>The flowering tree crateva religiosa (syn crateva adansonii) is called the<br>sacred garlic pear and temple plant, and many other names in a variety of<br>dialets, including Balai, lamok, abiyuch, barna, varuna and bidasi. The tree<br>is sometimes called the spider tree because the showy flower bear long,<br>spidery stamens. It is native to Japan, Australia, much of South East Asia<br>and several South east Asia and several South pacific islands. It is grown<br>elsewhere for fruit especially in part of African continent.<br>The crateva adansonii plant is a moderate sized, spreading unarmed,<br>deciduous tree growing to a height of 15 meters. Bark is grey, the wood<br>yellowish-white turning light brown when old. Leaves are clustered at the<br>end of the branchlets with a common petiole 5-10 centimeter long, at the<br>summit of which are three leaflets. Leaflets are ovate-lanceolate or ovate<br>7.5-12 centimeter long, 4-6 centimeter wide. Pointed at the base rather<br>slender pointer at the tip. Flower occur in terminal corymbs, about 5<br>centimeters in diameter, greenish yellow, and at length purplish.<br>Petals are ovate or oblong with the claw haft as long as the limb. Fruit is<br>ovoid or rounded, 3-5 centimeter in diameters, with a hard and rough rind. <br></p>

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