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51]

Review Article

Pain and inflammation: Management by

conventional and herbal therapy
David Arome, Akpabio Inimfon Sunday, Edith Ijeoma Onalike, Agbafor Amarachi1
Department of Science Laboratory Technology (Physiology and Pharmacology Technology), University of Jos, Plateau State, 1Biochemistry,
Covanent University, Ota, Ogun State, Nigeria

ABSTRACT
The sensation of pain is an indication that something is wrong somewhere in the body. Pain and inflammation may be linked by
cyclooxygenase (COX) enzymes most especially COX2, which help in the synthesis of prostaglandins (PGs) precisely PGE2 and PGF2a,
found in high concentration at the inflammatory site. The released PGs either stimulate pain receptor or sensitized pain receptors to the
action of other pain producing substances such as histamine, 5-hydroxytryptamine (5HT), bradykinin which initiate and cause the nerve
cells to send electrical pain impulse to the brain. In the present review, an attempt is made to unveil the treatment approach adopted in the
management of pain and inflammation as well as animal models used in evaluating herbal plants with analgesic and anti-inflammatory
properties. The choice of the use of herbal medicine have been encouraged due to it availability, affordability, accessibility, and little or no
side effect associated with it. However, the question remains can herbal therapy serves as an alternative to available conventional drugs.
Different treatment options in the management of pain and inflammation have been highlighted.
Key words: Conventional drugs, herbal medicine, inflammation, pain

body to react, for instance by withdrawing the hand from

a very hot object.[3]

Introduction
The sensation of pain is an indication that something
is wrong somewhere in the body. Pain in its real sense
has no precise definition, but in general term, occurs
whenever the body tissue is damaged.[1] The damage may
be superficial or deep right in the tissue of the body. The
function of pain is to draw attention to injury and through
the reflexes elicited to protect the injured part. Whenever
pain sets in, the individual reacts to remove the pain.
Pain receptors and aerent pain fibers are distributed
all round the body. The pain sensation is initiated by
peripheral receptors by stimuli: Such as mechanical,
thermal, electrical, chemical, etc., at a threshold sucient
to cause tissue damage.[2] The pain stimulus is processed
in the brain which then sends impulses down the spinal
cord and through appropriate nerve which commands the

Inflammation is a natural response of the body to a variety

of hostile agents; invading microbes, physical injury,
and toxic substances which lead to the accumulation
of blood and plasmatic body f luids.[4] Inf lammation is
a normal protective mechanism adopted by the body
to get rid of offending stimuli, but if not properly
treated may result to a more damage with exuberance
to create chronic inf lammation,[5] and other diseases.[6]
Inf lammation is characterized by five cardinal clinical
signs, namely redness, swelling, pain, heat, and loss
of function.[7] Inf lammation can be acute and chronic.
Inf lammation is the most frequent triggered of pain.
Pain is basically triggered in an inf lamed tissue by
arachidonic acid metabolism as well as other painproducing substances released from the damaged

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DOI:
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Indian Journal of Pain | January-April 2014 | Vol 28 | Issue 1

Address for correspondence:

Mr. David Arome,
Department of Science Laboratory Technology,
(Physiology and Pharmacology Tech),
University of Jos - 23473, Nigeria.
E-mail: davearome@gmail.com
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Arome, et al.: Conventional and herbal therapy for pain and inflammation

tissue. [8] Inf lammation and pain may be linked by

cyclooxygenase (COX) enzymes most especially COX2
which help in the synthesis of prostaglandins (PGs)
precisely PGE2 and PGF2a, found in high concentration
at the inf lammatory site. [9] The released PGs either
stimulate pain receptor or sensitized pain receptors
to the action of other pain producing substances
such as histamine, 5-hydroxytryptamine (5HT), and
bradykinin which initiate and cause the nerve cells to
send electrical pain impulse to the brain.
Previous reports have implicated herbal medicine as
an alternative therapy to conventional drugs. Herbal
preparations are used for wide range of diseases such
as pain and inflammation with little or no side eect
associated with their use. The uses of conventional
drugs in the treatment of pain and inflammation have
largely been greeted with side eects. These presenting
challenges have triggered scientific researchers all over the
world in search of alternative therapy. The present work
seek to review the treatment approach adopted in the
management of pain and inflammation as well as animal
models used in evaluating herbal plants with analgesic and
anti-inflammatory properties.

Types of Pain
Fast Pain
This is a localized pricking type of pain felt less than
a second after application of pain stimulus: Electrical,
thermal, and stimuli. This type of pain is superficial and
is not felt in most deep part of the body tissue. Fast pain
is transmitted in the peripheral nerves to the spinal cord
through a nerve called A delta fibers (Ad fibers) at a speed
of 5-30 m/s. The high conductive velocity of pain stimulus
allows the body to withdraw immediately from the painful
and harmful stimuli in order to avoid further damage. For
example, touching hot plate and pin pricking.[2]
Slow Pain
Slow pain is a throbbing, diused, slow burning pain felt
few seconds after pain stimulus is applied and may last
for minutes, weeks, and even resulting to chronic pain
if not properly processed by the body. Slow pain starts
immediately after fast pain subsides. It is felt mostly in
deep tissue of the body. Slow pain is transmitted by C-fibers
(with diameter 0.2 and one thousand of a millimeter) to
the brain at a velocity of 0.5-2 m/s. The response of the
body is to hold the aected body part immobile so that
healing can take place. Other types of pain are: Referred
pain, viscera pain, etc.[2]
6

Differences between of fast pain and slow pain

Slow pain
Transmitted by very thin nerve
fibers
Poorly localized
All internal organs (except the
brain)
Body wants to be immobile to
allow healing (guarding, spam,
and rigidity)
Effective relief from opioid
Pain often radiates or is referred
For example, labor pain.

Fast pain
Transmitted by relatively thicker
faster conducting nerve fibers
Well localized
Mainly skin, mouth, and anus
Immediate withdrawal of
stimulation to avoid further
damage
Little relief from opioid
Pain does not radiate
For example, pain from a surgical
incision[10]

Pain transmission in the spinal cord and brain

Pain stimulus is transmitted through peripheral nerves to
the spinal cord and from there to the brain. This happens
via two dierent types of nerve fibers: Fast pain fibers and
slow pain fibers.
Fast pain is transmitted by A fibers to the spinal cord. Fast
pain fiber terminates at luminal one of the dorsal horns
of the spinal cord and excite the 2nd order neuron of the
neospinothalamic pathway which terminates at the reticular
area of the brainstem (ventrobasal complex). Fast pain
impulses are transmitted to specific and limited area of the
brain surface of cortex by neurotransmitter called glutamate
secreted by the fast pain nerve ending of the spinal cord
allowing for a relative precise localization of the pain.[3]
Slow Pain impulses are distributed diusely to dierent
parts of the brain. Each area of the brain elicit dierent
responds which explain the whole range of the symptoms
that pain can cause such as suering, sleeping diculties.[3]
Opioid analgesic system of the brain
The components of the opioid analgesic system of the
brain are:
1. The periaqueductal grey and periventricular area of the
mesencephalon in the upper pons
2. The raphe magnus nucleus located in the lower
pons and upper medulla and nucleus reticularis
paragigantocellaris.
3. Pain inhibitory complex located in the dorsal horn of
the spinal cord.
The nerve endings of the periaqueductal and periventricular
grey secrete mostly enkephalin, serotonin, when
stimulated. The endogenous mediator blocks signal at both
presynaptic and postsynaptic fibers of the Ad and C-fibers.
Met, leu enkephalin, dynorphin, and endorphin are the
major endogenous opioid substances found in the brain. The
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Arome, et al.: Conventional and herbal therapy for pain and inflammation

arrival of pain impulses to the brain stimulate the release

of stored opioids causing them to bind to the receptors of
the terminal end of the ascending pain stimulating fibers
(APSF) to block the transmission and perception of pain.[2]
Inflammation
Previous reports have shown that inf lammation
manipulates two proteins namely: Calcium-activated
chloride channel and M-type potassium channel found
at the damage tissue of the pain sensing terminals of the
nerve cells. These proteins when targeted by bradykinin
cause the nerve cells to send electrical pain impulse to the
brain. The underlying mechanism to which this electrical
signal is generated still remains unclear.[10]
Walling o eect of inflammation
The very first eect of inflammation is to wall o the
injured area from other part of the tissue. This is made
possible by the fibrinogen clots which prevent fluid from
reaching the injured area. The important of walling o
process is to delay or slow down the spread of bacterial
and other toxic products.[2]
Types of inflammation
1. Acute inflammation: This is the initial response of the body
to harmful stimuli. The stimuli increased the movement
of plasma and white blood cells to the injured area.
2. Chronic inf lammation: This occurs as a result of
inflammation being prolonged for a period of time.
Some time it may result to autoimmune disease. Other
less common types are subacute inflammation and
granulomatous chronic inflammation.
Subacute inflammation has a chronic sign similar to acute
and chronic inflammation. It is an intermediate stage
between the two major types of inflammation.
Granulomatous chronic inflammation is a special type
of chronic inflammation associated with tuberculosis.[3]
Characteristics of Inflammation
Inflammation is characterized by
a. Vasodilation of the blood vessel and increase in blood
flow due to release of vasodilators.
b. Increase in permeability of capillaries leading to leakage
of fluid into the interstitial spaces.
c. Fluid clotting in the interstitial space due to the
leakage of excess fibrinogen and other proteins from
the capillaries.
d. Movement of large granulocyte monocyte to the injured
tissue.
e. Swelling of the tissue cells.[2]
Indian Journal of Pain | January-April 2014 | Vol 28 | Issue 1

Inflammatory reactions
Inflammatory reaction has two components
1. Innate response
The innate response is activated immediately after
infection or microbes invade the body. Innate responses
also prevent the adaptive response from targeting
and destroying the host cell. Innate response consists
of vascular and cellular element. Innate response is
mediated by antigen presenting cells (APC) which is
made up of dendritic cells and microphages. APC ingest
and process the antigen and present it on the surface of
the lymph nodes
2. Adaptive immune response
This is a complementary response that follows after
pathogen has been recognized by the innate system. It is
mediated by T and B lymphocyte.
Inflammatory reactions is controlled by the following
system: Cytokines complement, kinin, and fibrinolytic
pathways by lipid mediators (PG and leukotrienes)
released from a dierent cells and vasoactive mediator
release from mast cells, basophils, and platelet.[3]
Models of pain and inflammation
1. Animal models for pain
Models for Peripherally Acting Drugs
a. Acetic acid reduced abdominal writhing in mice
This is a widely used experimental model for screening
peripherally acting analgesic agents. Mice of either sex of
weight 20-25 g are used. The animals are pretreated with
the test sample. Thirty minutes after pretreatment, 0.2 ml
of 1% of the prepared acetic acid is injected into the animals
through intraperitoneal (IP) route, after which the mice
are transferred into a plastic bucket and observed. The
number of full abdominal writhes is counted for a total
duration of 5 min for each mouse.[11]
b. Pain in inflamed tissue (Randall-Selitto test)
The principle of this method is based on the fact
that inflammation increases the peripheral analgesic
sensitivity to pain. Animal with weight range of 130175 g fasted for 18-24 h is used. 0.1 ml of 20% suspension
of Brewers yeast is injected subcutaneously into the
left hind planter side of the paw. Three hours after
pretreatment with the test agent, pressure is applied
through tip of the plantar surface of the rat foot as
a constant rate using analgesiometer. Animal with a
control pain threshold greater than 80 g is eliminated
and replaced.[12]
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Arome, et al.: Conventional and herbal therapy for pain and inflammation

Models for centrally acting drugs

a. Tail immersion test
Animals used for the test are placed in an individual
cage or restrainer, allowing for 30 min of acclimatization
leaving the tail hanging out freely. Five centimeter from
its tips of the animal tail is marked. The marked part is
immersed in cup of freshly filled water of temperature of
55C. Stopwatch is used in recording the reaction time,
both before and after administration of the test compound.
Withdrawal time more of than 6 s is regarded as a positive
response.[13]
b. Hot plate test
Hot plate test is used to assay narcotic drugs or agents. In
this method, hot plate surface is maintained at a constant
temperature of 55-56C. Animals are placed in a glass
bucket of 55 cm diameter or heated surface, and the
time between placement and shaking or leaking of the
paw or jumping is recorded as index of response latency.
Animals receive the test compound orally 1 h before they
are placed on the hot plates. Centrally acting analgesic
drug prolonged the response time.[14]
Other models for centrally analgesic drugs are:
1. Pleurisy test
2. Ultraviolent erythema test in guinea pigs
3. Oxazolone-induced ear edema in mice
4. Granuloma pouch techniques
Animal models for inflammation
Experimental models for acute and subacute inflammation
study
a. Carrageenan-induced paw edema in rat
This model is used to assay acute anti-inflammatory activity
of a test agent. One hour after pretreatment of animals with
test sample, 0.1 ml of 1% prepared carrageenan is injected
subcutaneously into plantar side of the left hind paw of
the animal. Paw volume is measured at 30 min interval
after the injection of 0.1 ml prepared carrageenan for
the total duration of 2-3 h, paw volume of the animal is
measured at 0 min with digital plethysmometer before the
administration of the test sample. The dierence between
the initial and subsequent paw volume values gives the
actual paw edema and which compared with the control.
Paw volume can also be measured with vernier caliper, pair
of divider, and cotton thread.[15]
b. Egg albumin induce paw edema in rat
Egg albumin is used to screen agent with acute antiinflammatory eects, especially if inflammation is not
intended to be sustained for long. The procedure used
is the same as that of the carrageenan, but with slight
8

modification in some cases. Here paw volume is measured

as 20 min interval after the injection of 0.1 ml of the egg
albumin for the total duration of 2 h. Paw volume is
measured at 0 min before the administration of the test
compound.[16]

Treatment of Pain and Inflammation

1.
2.
3.
4.

Nonsteroidal anti-inflammatory drugs (NSAIDs)

Narcotic drugs
Corticosteroids drugs
Immune selective anti-inf lammatory derivatives
(mSAIDs)
5. Herbal therapy
NSAIDs
NSAIDs are used for the treatment of mild to moderate
type of pain and inflammation. For example, ibuprofen,
indomethacin, and diclofenac. NSAIDs act through
inhibition of enzyme COX, most precisely COX 2
responsible for the biosynthesis of PGs which triggered
inflammation thereby preventing the amplification of the
pain stimuli.[17,18]
Side effects: Nausea, indigestion, bleeding from the
stomach, peptic ulcer, and bronchopasm.[19]
Narcotics Drugs
Basically used in the treatment of severe type of pain. These
are classified into three groups:
i. Natural opium alkaloid divided into
a. Phenanthrene group: For example, morphine
b. Benzylisoquinoline group: For example, papaverine
ii. Semisynthetic opioid: For example, oxycodone
iii. Synthetic derivatives with structures unrelated to
morphine
Mechanism of action
The pharmacological action of narcotic is mediated
by specific and multiple receptors. mainly: d, m,
and k receptors. Stimulation cause the release of the
endogenous opioids like enkaphalin, dynorphin from
the terminal ending of the descending pain inhibitory
fibers making to attached to receptors of the terminal of
the ascending pain carry fibers, and prevent the release
of substance P. All opioid analgesic receptors bind to
selective endogenous opioid receptors to elicit their
pharmacological action.[3]
Side effect of narcotics analgesic drugs: Euphoria,
tolerance, nausea, vomiting, and sedation.
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Arome, et al.: Conventional and herbal therapy for pain and inflammation
Table 1: Herbal plants with analgesic and anti-inflammatory property
Plant (family)
Ficus ingens
(Moraceae)

Part used
Leaves

Zea may Husk

(Poacea)
Carica papaya

Seeds

Typhonium
Leaves
trilobatum
(Araceae)
Dracaena cinnabari Resin
Balf
Kaempferia galanga Rhizomes

Stachys
lavandulifolia

Aerial
parts

Jatropha curcas

Leaves

Tabernaemontana
divaricata
(Apocynaceae)

Flower

Tectona grandis
(Verbenaceae)
Guiera
senegalensis Gmel
(Combretaceae)

Leaves
Leaves

Litsea sebifera
(Lauraceae)

Different
part

Markhamia
tomentosa
(Bignoniaceae)

Leaves

Rosa damascene
(Rosaceae)

Chemical constituents
Alkaloids, glycosides, saponins,
flavonoids, carbohydrates,
tannins
Tannins, steroids, polyphenols

Uses
Fever, pain, inflammation,
pile, diarrhea, diuretics

Alkaloids, resins,
carbohydrates, fats, glycosides
Reducing sugar, alkaloids,
flavonoids, steroids tannins,
flavonoids gums, glycosides
Flavonoids, trepenoids, sterol

Antibacterial, malaria,
inflammation, deworming
Piles, rheumatism, asthma,
head ache, gastric ulcer

Pain, arthritis

Gastric sores, diarrhea,

dysentery, analgesic, skin
and mucosal diseases
Volatile oils: Eucalyptol,
Abdominal pain,
carvone
embrocation applied
on muscular swelling,
rheumatism
Flavonoids, saponins, and bitter Pain, inflammatory disorders
compounds

Animal models
References
Hot plate test, acetic acid-induced [11,14,23]
writhing test, carrageenaninduced paw edema
[24-28]
Hot plate test, formalin-induced
paw licking test, carrageenaninduced paw edema
[29-31]
Fresh egg albumin
Acetic acid-induced writhing,
xylene-induced ear edema

Acetic acid test, tail flick,

carrageenan-induced paw edema,
trauma-induced paw edema
Hot plate test, radiant heat tail
flick, carrageenan-induced paw
edema, cotton pellet-induced
granuloma model
Acetic acid-induced writhing,
formalin test, light tail flick,
carrageenan-induced paw edema
Alkaloids, saponins, trepenoids, Jaundice, pain, skin diseases, Acetic acid writhing test, egg
tannins, and steroids
cancer, snake bites
albumin-induced edema
Alkaloids, glycosides, steroids, Rejuvenation therapy, pain
Acetic acid-induced writhing, hot
saponins, flavonoids, terpenes, and inflammation, improved plate reaction test, carrageenanglycosides, proteins, amino
memory
induced paw edema
acids, fixed oil, tannins, and
volatile oil
Flavonoids, phenolic acids,
Analgesic, inflammation,
Eddys hot plate, carrageenanquinines, terpenes
wound healing
induced paw edema model
Alkaloids, glycosides, tannins, Diarrhea, rheumatism,
Acetic acid-induced writhing test,
and flavonoids
syphilis, leprosy, impotence, egg albumin induced edema,
dieresis, expurgation, fever,
malaria
Alkaloids, flavonoids,
Antiseptic, expectorant,
Acetic acid-induced writhing
glycosides, and saponins
tonics, fever, pain,
in mice, formalin induced hind
inflammation
paw licking test, carrageenaninduced paw edema, egg albumin
inflammation
Tannins, alkaloids, cardiac
Rheumatoid arthritis,
Writhing test, hot plate test,
glycosides, flavonoids, phenol, edema, gout, headache,
formalin test, immersion test,
an saponins
snake venom, scrotal
carrageenan
elephantiasis
Flavonoids, glycosides, tannins, Inflammatory diseases,
Writhing test, formalin test, tail
quercetin, caempterol, terpene, cough remedy, digestive
flick test, formalin-induced paw
myrcene, vitamin C, carboxylic, problems, laxative,
licking test, carrageenan-induced
essential oil: Geraniol,
antibacterial activity
paw edema
docosane, beta-citronellol, and
nonadacene

Corticosteroid Drugs
These are anti-inf lammatory agents that prevent
phospholipid release and undermines eosinophil action and
number of other mechanism involved in inflammation.[10]
Sets of corticosteroids drugs
a. Glucocorticoids are normally prescribed in the
treatment of inflammatory bowel diseases, hepatitis,
and allergic reactions.
Indian Journal of Pain | January-April 2014 | Vol 28 | Issue 1

[32-35]

[15,36-43]

[1,6,44-47]

[11,14,15,48]

[49,50]

[15,51,52]

[53-60]

[61-63]

[64-67]

[14,15,68-71]

[14,15,72-76]

b. Mineralocorticoid: Used with other medications in the

treatment of cerebral salt wasting.
mSAIDs
This new class of anti-inflammatory agent is found to alter
the activation and migration of immune cells involved
in amplification of inf lammatory response. mSAIDs
have been implicated as potential veterinary drugs for
controlling and reducing inflammation.[10]
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Arome, et al.: Conventional and herbal therapy for pain and inflammation

Herbal Therapy
Herbal medicine is the oldest form of healthcare known
to mankind. Herbs have been used virtually by all culture
throughout history. People around the world in dierent
civilization have used plants to treat dierent diseases for
several years.[20] Herbal medicine is an alternate treatment
of disease which constitutes the use of dierent plants and
their extracts. Herbal medicine comes in dierent forms
that include extract, tablet, essential oil, or ointment.
Herbs are used to treat various disease conditions such
as asthma, eczema, premenstrual syndrome, etc., and
some cases may have fewer side eects than conventional
drugs.[21] About 28% of all modern drugs in use today are
derived directly from naturally occurring substances in
plants.[22] Substances derived from plants remain the basis
for large proportion of commercial medication Table 1.

5.
6.

7.

8.
9.

10.
11.

Conclusion

12.

Inflammation is a normal defensive mechanism adopted

by the body to get rid of invading microbes. However,
if left untreated may result to other chronic diseases.
Hence, there is need to arrest it before it gets out of
control. Dierent treatment options are available in the
treatment of pain and inflammation. Conventional and
herbal therapies are the widely used options employed.
The use of the former is greeted with numerous unwanted
side eects, which limit their application. The choice of
the use of herbal medicine have been encouraged due to it
availability, aordability, accessibility, and little or no side
eect associated with it.

13.

14.
15.

16.

17.

18.

The use of herbal medicine can serve as treatment options

or alternative therapy in the treatment of pain and
inflammation.

19.

Acknowledgment

20.

The authors would sincerely like to appreciate Mr Imadi David for

his encouragement and support toward the success of this paper.

21.

References

22.

1.

23.

2.
3.
4.

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How to cite this article: Arome D, Sunday AI, Onalike EI, Amarachi
A. Pain and inflammation: Management by conventional and herbal
therapy. Indian J Pain 2014;28:5-12.
Source of Support: Nil. Conflict of Interest: None declared.

Indian Journal of Pain | January-April 2014 | Vol 28 | Issue 1