Evalution seminor on inflammation

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DEPARTMENT OF PHARMACOLOGY, PESCP, 14/4/2017 Page 1
SEMINAR
ON
INFLAMMATION
IN
ADVANCED PHARMACOLOGY AND TOXICOLOGY
SUBMITTED BY:-
MANU S J
1ST
M pharm
DEPARTMENT OF PHARMACOLOGY
SUBMITTED TO:-
Dr. SHIVALINGE GOWDA KP
ASSOCIATE PROFESSOR AND HOD
DEPARTMENT OF PHARMACOLOGY,
PES COLLEGE OF PHARMACY
HANUMANTHANAGAR, 50 FT ROAD,
BENGALURU, KARNATAKA-560050
BENGALURU

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This is certify that Mr. Manu S J has submitted the hard copy of the seminar topic
entitled “ Inflammation” and he has presented this seminar on 15/4/2017 at the
department of Pharmacology, PES college of pharmacy, Bangaluru-50 in the
subject of “ADVANCED PHARMACOLOGY AND TOXICOLOGY” in
Masters of pharmacy (Part-1), for the year 2017-18.
Signature of the subject in charge:-
Date:- 15/4/2017 Dr. Shivalinge Gowda K P.
Associate Professor and HOD
PES College of Pharmacy

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Introduction
Inflammation is a physiological mechanism of the response of the organism to the injury.
Excessive generation of inflammatory mediators has been linked to tissue damage and
compromised tissue repair process. Acute and chronic inflammations are therefore essential to
many diseases and pathological conditions such as atherosclerosis, heart failure, cancer,
thrombosis and many others.1
Based on visual observation, the ancients characterized inflammation by five cardinal signs,
namely redness (rubor), swelling (tumour), heat (calor; only applicable to the body' extremities),
pain (dolor) and loss of function (functio laesa). More recently, inflammation was described as
"the succession of changes which occurs in a living tissue when it is injured provided that the
injury is not of such a degree as to at once destroy its structure and vitality".2
The initial inflammation phase consists of three sub-phases: acute, sub-acute, and chronic (or
proliferative). The acute phase typically lasts 1–3 days and is characterized by the five classic
clinical signs: heat, redness, swelling, pain, and loss of function. The sub-acute phase may last
from 3–4 days to 1 month and corresponds to a cleaning phase required before the repair phase.
If the sub-acute phase is not resolved within 1 month, then inflammation is said to become
chronic and can last for several months. Tissue can degenerate and, in the loco-motor system,
chronic inflammation may lead to tearing and rupture. Alternatively, after the sub-acute
inflammatory phase, tissue can repair and be strengthened during the remodeling phase.3
Causes of Inflammation4
Microbial infections
One of the most common causes of inflammation is microbial infection. Microbes Include
viruses, bacteria, protozoa, fungi and various parasites. Viruses lead to death of Individual cells
by intracellular multiplication, and either cause the cell to stop Functioning and die, or cause
explosion of the cell (cytolytic), in which case it also dies. Bacteria release specific toxins –
either exotoxins or endotoxins.

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Hypersensitivity reactions
A hypersensitivity reaction occurs when an altered state of immunologic responsiveness Causes
an inappropriate or excessive immune reaction that damages the tissues.
Physical agents, irritant and corrosive chemicals
Tissue damage leading to inflammation may occur through physical trauma, ultraviolet or Other
ionizing radiation, burns or excessive cooling ('frostbite'). Corrosive chemicals (Acids, alkalis,
oxidizing agents) provoke inflammation through direct tissue damage. These chemical irritants
cause tissue damage that leads directly to inflammation.

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Tissue necrosis
Death of tissues from lack of oxygen or nutrients resulting from in-adequate blood flow is a
potent inflammatory stimulus.
Pathophysiology of inflammation
From a pathological point of view, the acute response to tissue injury occurs in the
microcirculation at the site of injury. Initially, there is a transient constriction of arterioles;
however, within several minutes, chemical mediators released at the site relax arteriolar smooth
muscle, leading to vasodilation and increased capillary permeability. Protein-rich fluid then
exudes from capillaries into the interstitial space. This fluid contains many of the components of
plasma including albumin, fibrinogen, kinins, complement, and immunoglobulins that mediate
the inflammatory response.
The sub-acute phase is characterized by movement of phagocytic cells to the site of injury. In
response to adhesion, molecules released from activated endothelial cells, leukocytes, platelets,
and erythrocytes in injured vessels become sticky and adhere to the endothelial cell surfaces.
Polymorphonuclear leukocytes such as neutrophils are the first cells to infiltrate the site of
injury. Basophils and eosinophils are more prevalent in allergic reactions or parasitic infections.
As inflammation continues, macrophages predominate, actively removing damaged cells or
tissue. If the cause of injury is eliminated, the sub-acute phase of inflammation may be followed
by a period of tissue repair. Blood clots are removed by fibrinolysis, and damaged tissues are
regenerated or replaced with fibroblasts, collagen, or endothelial cells. During the remodeling
phase, the new collagen laid down during the repair phase (mainly type III) is progressively
replaced by type I collagen to adapt to the original tissue. However, if inflammation becomes
chronic, further tissue destruction and/or fibrosis occurs.2

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ACUTE INFLAMMATION
In the early stages of inflammation, the affected tissue becomes reddened, due to increased blood
flow, and swollen, due to edema fluid. These changes are the result of vascular response to
inflammation. The vascular events of the acute inflammatory response involve three main
processes:
1. changes in vessel caliber and, consequently, blood flow (hemodynamics)
2. increased vascular permeability and
3. formation of the fluid exudate
1. Changes in Vessel Caliber
The microcirculation consists of the network of small capillaries lying between arterioles, which
have a thick muscular wall, and thin-walled venules. Capillaries have no smooth muscle in their
walls to control their caliber, and are so narrow that red blood cells must pass through them in
single file. The smooth muscle of arteriolar walls forms pre-capillary sphincters that regulate
blood flow through the capillary bed. Flow through the capillaries is intermittent, and some form
preferential channels for flow while others are usually shut down. In other words, there is not

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blood flowing through all capillaries all the time. They take turns. When inflammation happens,
none of them gets to take their scheduled tea break. They are all open.
Experimental evidence indicates that blood flow to the injured area may increase up to ten-fold
as vessels dilate. What causes this to happen? MEDIATORS - including nitric oxide, histamine
and prostaglandins (PGI2) and LTB4.
2. Increased vascular permeability
In acute inflammation, the capillary hydrostatic pressure increases, and there is also escape of
plasma proteins into the extravascular space due to increased vascular permeability (endothelial
contraction allowing proteins to escape between cells). Consequently, much more fluid leaves
the vessels than is returned to them. The net escape of protein-rich fluid is called exudation;
hence, the fluid is called an exudate.
There are two mechanisms which increase the vascular permeability
Chemical mediators of acute inflammation may cause retraction of endothelial cells,
leaving intercellular gaps (chemical mediated vascular leakage).
Toxins and physical agents may cause necrosis of vascular endothelium, leading to
abnormal leakage (injury induced vascular leakage).
3. Formation of the Cellular Exudate
white blood cells get out of the circulation and into the area

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Cells are called out to the area of inflammation in a process called CHEMOTAXIS.
Chemotaxis of leukocytes
The movement of leukocytes from the vessel lumen in a directional fashion to the site of tissue
damage is called chemotaxis. All granulocytes and monocytes respond to chemotactic factors
and move along a concentration gradient (from an area of lesser concentration of the factor to an
area of greater concentration of the factor).

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Chronic Inflammation
Chronic inflammation, like its acute cousin, is a host response to an inciting stimulus. There are,
however, some distinct differences. First and foremost is the time factor. Chronic inflammation
is considered to be inflammation of prolonged duration - weeks to months. Second, rather than
being just exudative, chronic inflammation usually is productive or proliferative. Cells in the
chronic inflammatory process tend to produce substances that add new tissue, such as collagen
and new blood vessels. Many of these changes also represent the repair process and there is a
blurry continuum between chronic inflammation and the whole repair process. In general,
chronic inflammation is characterized by inflammation, tissue destruction, and attempts at repair
all happening at once.
Chronic inflammation tends to occur under the following conditions:
Infections by organisms which are resistant to killing and clearing by the body tend to cause
Chronic inflammation. Such persistent organisms include some of the higher bacteria (Including
mycobacteria), fungi, and quite a few metazoan parasites.
Repeated bouts of acute inflammation can result in a chronic reaction.
Prolonged exposure to toxins can cause chronic inflammation.
Chronic inflammation is a common component in many of the autoimmune diseases.
The chronic inflammation doesn’t ooze, rather its exudates tends to be kind of solid and White or
grayish and it looks the same no matter what the cell types, here are the cell types:
1. The simplest type of chronic inflammation has mostly lymphocytes with lesser numbers of
Macrophages. This will occur mostly in viral infections where the virus survives longer than
The acute phase. This is called “lymphohistiocytic”.
2. Chronic active inflammation is the same but in this one there are still some neutrophils
Present. This happens in many bacterial infections that are not due to very pus-producing
bacteria.
3. Next is granulomatous - here the cell types are almost all macrophages. Good examples
are fungal infections or mycobacteria.
4. Some people use a term pyogranulomatous - which means granulomatous but within the
macrophages are pockets of neutrophils.
5. Granulomas occur when the inciting cause stimulates macrophages but the agents are
Distributed discretely within an organ. Think TB. Think Blastomyces. Think foreign body.

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Granulomatous inflammation
There is one specific subset of chronic inflammation that deserves special attention, and that is
granulomatous inflammation. Histologically, it is very characteristic and is described below.
Granulomatous inflammation is any inflammatory response consisting predominantly of
Macrophages
A granuloma is a focally discrete chronic inflammatory reaction comprised Pre-dominantly
of epithelioid macrophages that are organized or aggregated in closely Packed collections.
There is often a central core of caseous debris at the center of the Granuloma surrounded
by macrophages that in turn are encircled by a ring of Lymphocytes and organizing
fibroblasts.
Chemical Mediators of Inflammation2
Biochemical mediators released during inflammation intensify and propagate the inflammatory
response. These mediators are soluble, diffusible molecules that can act locally and systemically.

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Mediators derived from plasma include complement and complement-derived peptides and
kinins. Released via the classic or alternative pathways of the complement cascade,
complement-derived peptides (C3a, C3b, and C5a) increase vascular permeability, cause
smooth muscle contraction, activate leukocytes, and induce mast-cell degranulation. C5a is a
potent chemotactic factor for neutrophils and mononuclear phagocytes. The kinins are also
important inflammatory mediators. The most important kinin is bradykinin, which increases
vascular permeability and vasodilation and, importantly, activates phospholipase A2 (PLA2) to
liberate arachidonic acid (AA). Bradykinin is also a major mediator involved in the pain
response.
Actions of Inflammatory Mediators
Action Mediatorsa
Vasodilation, increased
vascular permeability
Histamine, serotonin, bradykinin, C3a, C5a, LTC4, LTD4, PGI2,
PGE2, PGD2, PGF2, activated Hageman factor, kinonogen
fragments, fibrinopeptides
Vasoconstriction TXA2, LTB4, LTC4, LTD4, C5a
Smooth muscle contraction
C3a, C5a, histamine, LTB4, LTC4, LTD4, TXA2, serotonin, PAF,
bradykinin
Mast cell degranulation C5a, C3a
Stem cell proliferation IL-3, G-CSF, GM-CSF, M-CSF
Chemotaxis C5a, LTB4, IL-8, PAF, 5-HETE, histamine, others
Lysosomal granule release C5a, IL-8, PAF
Phagocytosis C3b, iC3b
Platelet aggregation TXA2, PAF
Endothelial cell stickiness IL-1, TNF-α, LTB4
Granuloma formation IL-1, TNF-α
Pain PGE2, bradykinin, histamine, serotonin
Fever IL-1, IL-6, TNF-α, PGE2

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Action Mediatorsa
a
C = complement, LT = leukotriene, PG = prostaglandin, TX = thromboxane, PAF = platelet
activating factor, IL = interleukin, CSF = colony stimulating factor, HETE =
hydroxyeicosatetranoate, TNF = tumor necrosis factor
Other mediators are derived from injured tissue cells or leukocytes recruited to the site of
inflammation. Mast cells, platelets, and basophils produce the vasoactive amines serotonin and
histamine. Histamine causes arteriolar dilation, increased capillary permeability, contraction of
nonvascular smooth muscle, and eosinophil chemotaxis and can stimulate nociceptors
responsible for the pain response. Its release is stimulated by the complement components C3a
and C5a and by lysosomal proteins released from neutrophils. Histamine activity is mediated
through the activation of one of four specific histamine receptors, designated H1, H2, H3, or H4,
in target cells. Most histamine-induced vascular effects are mediated by H1 receptors. H2
receptors mediate some vascular effects but are more important for their role in histamine-
induced gastric secretion. Less is understood about the role of H3 receptors, which may be
localized to the CNS. H4 receptors are located on cells of hematopoietic origin, and H4
antagonists are promising drug candidates to treat inflammatory conditions involving mast cells
and eosinophils (allergic conditions).
Serotonin (5-hydroxytryptamine) is a vasoactive mediator similar to histamine found in mast
cells and platelets in the GI tract and CNS. Serotonin also increases vascular permeability, dilates
capillaries, and causes contraction of nonvascular smooth muscle. In some species, including
rodents and domestic ruminants, serotonin may be the predominant vasoactive amine.
Cytokines, including interleukins 1–10, tumor necrosis factor α (TNF-α), and interferon γ (INF-
γ) are produced predominantly by macrophages and lymphocytes but can be synthesized by other
cell types as well. Their role in inflammation is complex. These polypeptides modulate the
activity and function of other cells to coordinate and control the inflammatory response. Two of
the more important cytokines, interleukin-1 (IL-1) and TNF-α, mobilize and activate leukocytes,
enhance proliferation of B and T cells and natural killer cell cytotoxicity, and are involved in the
biologic response to endotoxins. IL-1, IL-6, and TNF-α mediate the acute phase response and

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pyrexia that may accompany infection and can induce systemic clinical signs, including sleep
and anorexia.
The role of the free radical gas nitric oxide (NO) in inflammation is well established. NO is an
important cell-signaling messenger in a wide range of physiologic and pathophysiologic
processes. Small amounts of NO play a role in maintaining resting vascular tone, vasodilation,
and anti-aggregation of platelets. In response to certain cytokines (TNF-α, IL-1) and other
inflammatory mediators, the production of relatively large quantities of NO is stimulated. In
larger quantities, NO is a potent vasodilator, facilitates macrophage-induced cytotoxicity, and
may contribute to joint destruction in some types of arthritis.
MORPHOLOGIC DIAGNOSIS
1. Severity
Mild, moderate, severe
2. Time course
Peracute, acute, subacute, chronic
3. Distribution of lesion
Focal, Multifocal, ,Locally extensive, Diffuse
4. Type of Exudate
Difference between exudates and transudate
Serous, Fibrinous, Catarrhal, Purulent, Abscess, Hemorrhagic, Mixed
5. Inflammatory name associated with the organ- usually it is just-it is, but there are exceptions.

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Anti-inflammatory drugs
Nonsteroidal Anti-inflammatory Drugs
The importance of pain management and the use of NSAIDs in animals has increased
dramatically in recent decades, with use of NSAIDs in companion animals being routine.
NSAIDs have the potential to relieve pain and inflammation without the metabolic,
hemodynamic, and immunosuppressive adverse effects associated with corticosteroids.
However, all NSAIDs have the potential for other adverse effects that should be considered in
overall management of the inflammatory process.
Mode of Action:
Generally, the classification NSAID is applied to drugs that inhibit one or more steps in the
metabolism of arachidonic acid (AA). Unlike corticosteroids, which inhibit numerous pathways,
NSAIDs act primarily to reduce the biosynthesis of prostaglandins by inhibiting cyclooxygenase
(COX). In general, NSAIDs do not inhibit the formation of 5-lipoxygenase (5-LOX) and hence
leukotriene, or the formation of other inflammatory mediators. The novel NSAID tepoxalin is an
exception in that it inhibits both COX and 5-LOX.
The discovery of the two isoforms of COX (COX-1 and COX-2) has led to greater understanding
of the mechanism of action and potential adverse effects of NSAIDs. COX-1, expressed in
virtually all tissues of the body (eg, gut and kidney), catalyzes the formation of constitutive

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prostaglandins, which mediate a variety of normal physiologic effects, including hemostasis, GI
mucosal protection, and protection of the kidney from hypotensive insult. In contrast, COX-2 is
activated in damaged and inflamed tissues and catalyzes the formation of inducible
prostaglandin, including PGE2, associated with intensifying the inflammatory response. COX-2
is also involved in thermoregulation and the pain response to injury. Therefore, COX-2
inhibition by NSAIDs is thought to be responsible for the antipyretic, analgesic, and anti-
inflammatory actions of NSAIDs. However, concurrent inhibition of COX-1 may result in many
of the unwanted effects of NSAIDs, including gastric ulceration and renal toxicity. Because
NSAIDs vary in their ability to inhibit each COX isoform, a drug that inhibits COX-2 at a lower
concentration than that necessary to inhibit COX-1 would be considered safer. This concept has
propelled the development of the “COX-2 selective” NSAIDs. Although ratios of COX-1:COX-2
inhibition by various NSAIDs in people and animals have been reported, caution is advised when
interpreting such ratios, because they vary greatly depending on the selectivity assay used.
In general, drugs with ratios suggesting preferential activity against COX-2 may have fewer
adverse effects due to COX-1 inhibition. COX-1–sparing drugs are associated with less GI
ulceration and less platelet inhibition; however, it may be an oversimplification to assume that
complete COX-2 inhibition is without potential risk.
NSAIDs enter the pocket of the COX enzyme, whereupon steric hindrance prevents entry of AA.
Aspirin is unusual in that it irreversibly acetylates a serine residue of COX, resulting in a
complete loss of COX activity. Thus, the duration of the aspirin effect depends on the turnover
rate of COX; activity is lost for the life of the platelet (7–10 days) after aspirin administration,
explaining the duration of aspirin’s effect on hemostasis. Unlike aspirin, most other NSAIDs
(including salicylic acid, an active metabolite of aspirin) are reversible competitive COX
inhibitors; their duration of inhibition is primarily determined by the elimination
pharmacokinetics of the drug.

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Adverse Effects:
All NSAIDs have the potential to induce adverse reactions, some of which can be life
threatening. Many reactions to NSAIDs are dose-related and are typically reversible with
discontinuation of therapy and supportive care.
Vomiting is the most common adverse effect. GI ulceration is the most common life-threatening
adverse effect. NSAID-induced GI bleeding may be occult, leading to iron-deficiency anemia, or
be more severe, resulting in vomiting, hematemesis, and melena.
Aspirin:
By far the most widely used NSAID in people, aspirin is primarily used in veterinary medicine
for relief of mild to moderate pain associated with musculoskeletal inflammation or
osteoarthritis. The salicylic ester of acetic acid, aspirin (acetylsalicylic acid) is available in
several different dosage forms, including bolus (for cattle), oral paste (for horses), oral solution
(for poultry), and tablets (for dogs). Enteric-coated products used in human medicine are not
recommended in dogs, because gastric retention may lead to erratic plasma exposure. After PO
administration, aspirin is rapidly absorbed from the stomach and upper small intestine. Aspirin is
subjected to a large, first-pass effect in the liver to yield salicylic acid, its main active metabolite.
In addition, the aspirin fraction that gains access to the systemic circulation is also rapidly
hydrolyzed to salicylic acid with a half-life of ~15 min. After oral aspirin administration,
salicylic acid is considered the main active substance in the systemic circulation. Aspirin
primarily inhibits COX-1, whereas salicylic acid has more balanced COX-1/COX-2 activity. In
addition, aspirin may irreversibly bind to COX-1 through acetylation of a serine residue near the
enzyme active site. Because of this irreversible binding, the anticoagulant activity of aspirin lasts
far longer than its anti-inflammatory effect; a single aspirin dose of 20 mg/kg in a horse may
prolong bleeding for 48 hr. Depending on its route of administration, aspirin may have different
pharmacologic effects. For irreversible platelet COX-1 inhibition (to treat a thromboembolic
condition), aspirin given IV is more efficient than aspirin given PO because, for the same dose,
aspirin exposure is greater for the IV route of administration.

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After absorption, both aspirin and salicylate are widely distributed through most tissues and
fluids and readily cross the placental barrier. Approximately 80%–90% of salicylate is bound to
plasma proteins. Metabolism and elimination is via hepatic conjugation with glucuronic acid,
followed by renal excretion. Cats, which lack glucuronyl transferase, metabolize salicylates
slowly. In addition, salicylate metabolism is saturable and, if overexposure due to an aspirin
overdose occurs, plasma salicylate elimination may follow a zero order and slower elimination
kinetics. The elimination half-life of salicylic acid in cats approaches 40 hr, whereas it is ~7.5 hr
in dogs.
Acetaminophen:
Acetaminophen (paracetamol) is a para-aminophenol derivative with analgesic and antipyretic
effects similar to those of aspirin, but it has weaker anti-inflammatory effects than does aspirin
and other NSAIDs. The reason for this anomaly is that acetaminophen’s selective COX-2
inhibition is via enzyme reduction; the high levels of peroxides in areas of inflammation are
thought to interfere with COX-2 reduction peripherally, whereas the low peroxide levels in the
brain and spinal cord account for any centrally mediated analgesia. Acetaminophen does not
inhibit neutrophil activation, has little ulcerogenic potential, and has no effect on platelets or
bleeding time. The recommended dosage of acetaminophen in dogs is 10–15 mg/kg, PO, tid.
Dose-dependent adverse effects include depression, vomiting, and methemoglobinemia. Use in
cats is contraindicated because of their deficiency of glucuronyl transferase, which makes them
susceptible to methemoglobinemia and centrilobular hepatic necrosis.
Glucocorticoids5
Glucocorticoids are widely used for the suppression of inflammation in chronic inflammatory
diseases such as asthma, rheumatoid arthritis, inflammatory bowel disease and autoimmune
diseases, all of which are associated with increased expression of inflammatory genes. The
molecular mechanisms involved in this anti-inflammatory action of glucocorticoids is discussed,
particularly in asthma, which accounts for the highest clinical use of these agents.
Glucocorticoids bind to glucocorticoid receptors in the cytoplasm which then dimerize and
translocate to the nucleus, where they bind to glucocorticoid response elements (GRE) on

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glucocorticoid-responsive genes, resulting in increased transcription. Glucocorticoids may
increase the transcription of genes coding for anti-inflammatory proteins, including lipocortin-1,
interleukin-10, interleukin-1 receptor antagonist and neutral endopeptidase, but this is unlikely to
account for all of the widespread anti-inflammatory actions of glucocorticoids. The most striking
effect of glucocorticoids is to inhibit the expression of multiple inflammatory genes (cytokines,
enzymes, receptors and adhesion molecules). This cannot be due to a direct interaction between
glucocorticoid receptors and GRE, as these binding sites are absent from the promoter regions of
most inflammatory genes. It is more likely to be due to a direct inhibitory interaction between
activated glucocorticoid receptors and activated transcription factors, such as nuclear factor-
kappa B and activator protein-1, which regulate the inflammatory gene expression. It is
increasingly recognized that glucocorticoids change the chromatin structure. Glucocorticoid
receptors also interact with CREB-binding protein (CBP), which acts as a co-activator of
transcription, binding several other transcription factors that compete for binding sites on this
molecule. Increased transcription is associated with uncoiling of DNA wound around histone and
this is secondary to acetylation of the histone residues by the enzymic action of CBP.
Glucocorticoids may lead to deacetylation of histone, resulting in tighter coiling of DNA and
reduced access of transcription factors to their binding sites, thereby suppressing gene
expression. Rarely patients with chronic inflammatory diseases fail to respond to
glucocorticoids, although endocrine function of steroids is preserved. This may be due to
excessive formation of activator protein-1 at the inflammatory site, which consumes activated
glucocorticoid receptors so that they are not available for suppressing inflammatory genes. This
new understanding of glucocorticoid mechanisms may lead to the development of novel steroids
with less risk of side effects (which are due to the endocrine and metabolic actions of steroids).
'Dissociated' steroids which are more active in transrepression (interaction with transcription
factors) than transactivation (GRE binding) have now been developed. Some of the transcription
factors that are inhibited by glucocorticoid, such as nuclear factor-kappa B, are also targets for
novel anti-inflammatory therapies.
Xanthine oxidse inhibitor6
A xanthine oxidase inhibitor is any substance that inhibits the activity of xanthine oxidase, an
enzyme involved in purine metabolism. In humans, inhibition of xanthine oxidase reduces the

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production of uric acid, and several medications that inhibit xanthine oxidase are indicated for
treatment of hyperuricemia and related medical conditions including gout. Xanthine oxidase
inhibitors are being investigated for management of reperfusion injury.
References
1. Ana M S. New insights in the pathophysiology of inflammation. Biochemia
Madica.2011; 21:243-5.
2. Neville A P, Cliff W, Lan A. The journal of inflammation. Bio Med Central. 2004; 1(1):
3-4.
3. Scott H E. Pathophysiology of inflammation. Marck Sharp and Dohme Corp. 2016; 4(7):
1-7.
4. Barnes P J. Anti-inflammatory actions of glucocorticoids: Molecular mechanism.
Pubmed. 1998; 94(6): 557-72.
5. https://en.wikipedia.org/wiki/Xanthine_oxidase_inhibitor

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