Project Materials

PHYTOCHEMICAL AND ANTI-INFLAMMATORY PROPERTIES OF METHANOL EXTRACT OF CRATEVA ADANSONII STEM BARK

ABSTRACT

This study looked into the phytochemical and anti-inflammatory activities of methanol extracts of Crateva adansonii stem bark. Although a variety of edible and non-edible plant parts are employed in inflammatory treatment, Crateva adansonii stem bark has been extensively documented. For this study, fresh stem bark of Crateva adansonii was gathered from Asata community in Enugu State. The cuttings were validated at the Bioresource Development Centre. They were then dried at room temperature for one month in an open lab area, pulverised into powder, and weighed 460.6g using a beam balance. The powder was steeped in methanol for 24 to 48 hours to produce a methanol extract, which was then condensed into a paste at a temperature range of 30-550C in a water bath. The anti-inflammatory test was performed on a group of twenty mature wistar albino rats. The rats were placed into five groups of four albino rats apiece. They were given 3% tween-80 combined with dichloromethane extract of Crateva adansonii, while the control received 0.5ml of 3% tween-80. Acute inflammation was generated an hour after test chemicals were supplied by injecting egg albumin into the subplanter region of the right hind paw, and oedema was measured by mercury displacement over a period of 0-180 minutes. The anti-inflammatory impact was considerable within 30 minutes of generated oedema, with inhibition occurring in three phases: 0-30, 30-60, and 60-90. 90-120-180 minutes. Inhibition was greatest in the third phase. Crateva adansonii barks demonstrated anti-inflammatory properties by suppressing “prostaglandin” synthesis, an inflammatory mediator.

Chapter one

INTRODUCTION

Inflation is derived from the Latin term inflammare, which meaning “to set on fire.” It is a complicated biological response of vascular tissue to potentially damaging stimuli such as pathogens, damaged cells, and irritants.

Inflammation is the vascularised tissue’s response to local harm induced by many stimuli such as infections, chemicals and biochemical agents, thermal or other physical trauma, antigen-antibody interaction, and so on (Carol, 1994).

Wounds will not heal unless an inflammatory reaction is present, and mild infections will worsen. Though inflammation strives to reduce damage and restore function, some enzymes and toxic chemicals generated by phagocytic cells cause tissue harm.

The introduction of anti-inflammatory drugs has reduced the strength of inflammation, which had previously posed a threat to human life due to its complicated, multifaceted nature. Unlike opioids, which impact the central nervous system, anti-inflammatory medications or pharmaceuticals serve to relieve pain by suppressing inflammation.

It also prevents repairs and mitigates the effects of inflammation by working on the body’s reactions rather than directly attacking the causal culprit (Stedman, 2000).

These anti-inflammatory processes involve balancing pro-inflammatory acute-phase reactants (Russell et al. 2000), altering the biochemical pathway 78 forming prostaglandins by inhibiting the cyclooxygenase enzyme from catalysing the reaction, and suppressing, compensating, and correcting mechanical and structural abnormalities using assistive devices (Masumoto et al. 2009).

The inflammatory reaction is the oldest defence mechanism in terms of both phylogeny and ontogeny. Although immune system cells are broadly spread throughout the body, they are activated when an infection or tissue damage occurs. It is vital to concentrate them and their products at the point of injury.