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 Table of Contents  
Year : 2014  |  Volume : 28  |  Issue : 1  |  Page : 5-12

Pain and inflammation: Management by conventional and herbal therapy

1 Department of Science Laboratory Technology (Physiology and Pharmacology Technology), University of Jos, Plateau State, Nigeria
2 Department of Biochemistry, Covanent University, Ota, Ogun State, Nigeria

Date of Web Publication15-Mar-2014

Correspondence Address:
David Arome
Department of Science Laboratory Technology, (Physiology and Pharmacology Tech), University of Jos - 23473
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/0970-5333.128879

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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 COX 2 , 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.

Keywords: Conventional drugs, herbal medicine, inflammation, pain

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

How to cite this URL:
Arome D, Sunday AI, Onalike EI, Amarachi A. Pain and inflammation: Management by conventional and herbal therapy. Indian J Pain [serial online] 2014 [cited 2020 Jul 10];28:5-12. Available from: http://www.indianjpain.org/text.asp?2014/28/1/5/128879

  Introduction Top

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 afferent 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 sufficient 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 body to react, for instance by withdrawing the hand from a very hot object. [3]

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 fluids. [4] Inflammation 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 inflammation, [5] and other diseases. [6] Inflammation is characterized by five cardinal clinical signs, namely redness, swelling, pain, heat, and loss of function. [7] Inflammation can be acute and chronic. Inflammation is the most frequent triggered of pain. Pain is basically triggered in an inflamed tissue by arachidonic acid metabolism as well as other pain-producing substances released from the damaged tissue. [8] Inflammation and pain may be linked by cyclooxygenase (COX) enzymes most especially COX 2 which help in the synthesis of prostaglandins (PGs) precisely PGE2 and PGF2a, found in high concentration at the inflammatory 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 effect associated with their use. The uses of conventional drugs in the treatment of pain and inflammation have largely been greeted with side effects. 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 Top

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, diffused, 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 affected body part immobile so that healing can take place. Other types of pain are: Referred pain, viscera pain, etc. [2]

Differences between of fast pain and slow pain

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 different types of nerve fibers: Fast pain fibers and slow pain fibers.

Fast pain is transmitted by Aδ fibers to the spinal cord. Fast pain fiber terminates at luminal one of the dorsal horns of the spinal cord and excite the 2 nd 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 diffusely to different parts of the brain. Each area of the brain elicit different responds which explain the whole range of the symptoms that pain can cause such as suffering, sleeping difficulties. [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 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]


Previous reports have shown that inflammation 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 off effect of inflammation

The very first effect of inflammation is to wall off 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 off 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 inflammation: 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

  1. Vasodilation of the blood vessel and increase in blood flow due to release of vasodilators.
  2. Increase in permeability of capillaries leading to leakage of fluid into the interstitial spaces.
  3. Fluid clotting in the interstitial space due to the leakage of excess fibrinogen and other proteins from the capillaries.
  4. Movement of large granulocyte monocyte to the injured tissue.
  5. Swelling of the tissue cells. [2]

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 different 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 130-175 g fasted for 18-24 h is used. 0.1 ml of 20% suspension of Brewer's 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]

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 55°C. 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 55-56°C. 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 difference 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 anti-inflammatory effects, 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 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 Top

  1. Nonsteroidal anti-inflammatory drugs (NSAIDs)
  2. Narcotic drugs
  3. Corticosteroids drugs
  4. Immune selective anti-inflammatory derivatives (mSAIDs)
  5. Herbal therapy


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:

  1. Natural opium alkaloid divided into
    1. Phenanthrene group: For example, morphine
    2. Benzylisoquinoline group: For example, papaverine
  2. Semisynthetic opioid: For example, oxycodone
  3. 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.

Corticosteroid Drugs

These are anti-inflammatory agents that prevent phospholipid release and undermines eosinophil action and number of other mechanism involved in inflammation. [10]

Sets of corticosteroids drugs

  1. Glucocorticoids are normally prescribed in the treatment of inflammatory bowel diseases, hepatitis, and allergic reactions.
  2. Mineralocorticoid: Used with other medications in the treatment of cerebral salt wasting.


This new class of anti-inflammatory agent is found to alter the activation and migration of immune cells involved in amplification of inflammatory response. mSAIDs have been implicated as potential veterinary drugs for controlling and reducing inflammation. [10]

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 different civilization have used plants to treat different diseases for several years. [20] Herbal medicine is an alternate treatment of disease which constitutes the use of different plants and their extracts. Herbal medicine comes in different 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 effects 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].
Table 1: Herbal plants with analgesic and anti-inflammatory property

Click here to view

  Conclusion Top

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. Different 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 effects, which limit their application. 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.

The use of herbal medicine can serve as treatment options or alternative therapy in the treatment of pain and inflammation.

  Acknowledgment Top

The authors would sincerely like to appreciate Mr Imadi David for his encouragement and support toward the success of this paper. [76]

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