Inflammation and Natural Products

442 Pages·2021·9.322 MB·English

by  Sreeraj Gopi, Augustine Amalraj, Ajaikumar B. Kunnumakkara, Sabu Thomas

I N F L A M M AT I O N A N D
N AT U R A L P R O D U C T S
I N F L A M M AT I O N A N D
N AT U R A L P R O D U C T S
Edited by
SREERAJ GOPI
Aurea Biolabs (P) Ltd, Kolenchery, Cochin, Kerala, India
AUGUSTINE AMALRAJ
Aurea Biolabs (P) Ltd, Kolenchery, Cochin, Kerala, India
AJAIKUMAR KUNNUMAKKARA
Indian Institute of Technology Guwahati, Guwahati, Assam, India
SABU THOMAS
Mahatma Gandhi University, Kottayam, Kerala, India
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Contributors
Mohammad H. Abukhalil Department of Biology, Faculty of Science,
Al-Hussein Bin Talal University, Ma’an, Jordan
Augustine Amalraj R&D Centre, Aurea Biolabs (P) Ltd, Kolenchery,
Cochin, Kerala, India
Thahira Banu Azeez School of Sciences, Department of Home
Science, The Gandhigram Rural Institute-Deemed to be University,
Gandhigram, Dindigul, Tamil Nadu, India
A. Thahira Banu School of Sciences, Department of Home Science,
The Gandhigram Rural Institute—Deemed to be University,
Gandhigram, Dindigul, Tamil Nadu, India
May Bin-Jumah Department of Biology, College of Science, Princess
Nourah Bint Abdulrahman University, Riyadh, Saudi Arabia
Fernão C. Braga Department of Pharmaceutical Products, Faculty
of Pharmacy, Federal University of Minas Gerais (UFMG), Belo
Horizonte, Brazil
Ana Laura Tironi de Castilho Department of Structural and
Functional Biology, São Paulo State University (UNESP), Botucatu,
SP, Brazil
Muhammad Daniyal TCM and Ethnomedicine Innovation and
Development International Laboratory, School of Pharmacy,
Hunan University of Chinese Medicine, Changsha, China
Sreeraj Gopi Department of Polymer Technology, Gdansk University
of Technology, Gdańsk, Poland; R&D Centre, Aurea Biolabs (P) Ltd,
Kolenchery, Cochin, Kerala, India
N.S.K. Gowthaman Materials Synthesis and Characterization
Laboratory, Institute of Advanced Technology, Universiti Putra
Malaysia, Serdang, Selangor, Malaysia
Józef T. Haponiuk Chemical Faculty, Gdansk University of
Technology, Gdańsk, Poland
Joby Jacob R&D Centre, Aurea Biolabs (P) Ltd, Kolenchery, Cochin,
Kerala, India
Shintu Jude R&D Centre, Aurea Biolabs (P) Ltd, Kolenchery, Cochin,
Kerala, India
H.N. Lim Department of Chemistry, Faculty of Science, Universiti
Putra Malaysia, Serdang, Selangor, Malaysia
xiii
xiv Contributors
Janeline Lunghar School of Sciences, Department of Home Science,
The Gandhigram Rural Institute-Deemed to be University,
Gandhigram, Dindigul, Tamil Nadu, India
Tooba Mahboob Department of Medical Microbiology, Faculty of
Medicine, University of Malaya, Kuala Lumpur, Malaysia
Ayman M. Mahmoud Physiology Division, Department of Zoology,
Faculty of Science; Biotechnology Department, Research Institute
of Medicinal and Aromatic Plants, Beni-Suef University, Beni-Suef,
Egypt
Akhila Nair Department of Polymer Technology, Gdansk University
of Technology, Gdańsk, Poland; R&D Centre, Aurea Biolabs (P) Ltd,
Kolenchery, Cochin, Kerala, India
Anjana S. Nair R&D Centre, Aurea Biolabs (P) Ltd, Kolenchery,
Cochin, Kerala, India
Veeranoot Nissapatorn School of Allied Health Sciences, Southeast
Asia Water Team (SEA Water Team) and World Union for Herbal
Drug Discovery (WUHeDD), Walailak University, Nakhon Si
Thammarat, Thailand
Diego P. de Oliveira Department of Pharmaceutical Products, Faculty
of Pharmacy, Federal University of Minas Gerais (UFMG), Belo
Horizonte, Brazil
Anupam Paliwal R&D Centre, Aurea Biolabs (P) Ltd, Kolenchery,
Cochin, Kerala, India
Jithin Raj R&D Centre, Aurea Biolabs (P) Ltd, Kolenchery, Cochin,
Kerala, India
Chandramathi Samudi Raju Department of Medical Microbiology,
Faculty of Medicine, University of Malaya, Kuala Lumpur, Malaysia
Ariane Leite Rozza Department of Structural and Functional Biology,
São Paulo State University (UNESP), Botucatu, SP, Brazil
Cristina C. Salibay College of Science and Computer Studies, De La
Salle University-Dasmariñas, Dasmariñas, Cavite, Philippines
Jonnacar S. San Sebastian College of Science and Computer
Studies, De La Salle University-Dasmariñas, Dasmariñas, Cavite,
Philippines
Matheus Chiaradia de Souza Department of Structural and
Functional Biology, São Paulo State University (UNESP), Botucatu,
SP, Brazil
Hazel Anne Tabo College of Science and Computer Studies, De La
Salle University-Dasmariñas, Dasmariñas, Cavite, Philippines
Carolina Mendes Tarran Department of Structural and Functional
Biology, São Paulo State University (UNESP), Botucatu, SP, Brazil
Contributors xv
Leonardo de Liori Teixeira Department of Structural and Functional
Biology, São Paulo State University (UNESP), Botucatu, SP, Brazil
Mauro M. Teixeira Department of Biochemistry and Immunology,
Institute of Biological Sciences, Federal University of Minas Gerais
(UFMG), Belo Horizonte, Brazil
Roshin U. Thankachen Department of Polymer Technology, Gdansk
University of Technology, Gdańsk, Poland
Bincicil Annie Varghese R&D Centre, Aurea Biolabs (P) Ltd,
Kolenchery, Cochin, Kerala, India
Karthik Varma R&D Centre, Aurea Biolabs (P) Ltd, Kolenchery,
Cochin, Kerala, India
Ajoy Kumar Verma National Institute of Tuberculosis and
Respiratory Diseases (NITRD), New Delhi, India
Wei Wang TCM and Ethnomedicine Innovation and Development
International Laboratory, School of Pharmacy, Hunan University of
Chinese Medicine, Changsha, China
Mateus Souza Zabeu Department of Structural and Functional
Biology, São Paulo State University (UNESP), Botucatu, SP, Brazil
1
Inflammation, symptoms,
benefits, reaction, and
biochemistry
Akhila Naira,b, Roshin U. Thankachena, Jithin Rajb,
and Sreeraj Gopia
aDepartment of Polymer Technology, Gdansk University of Technology,
Gdan’sk, Poland, bR&D Centre, Aurea Biolabs (P) Ltd, Kolenchery, Cochin,
Kerala, India
1.1 Introduction
The term inflammation is known from the Old Testament biblical
era when Moses mentions that “If the bright spot stay in his place, and
spread not in the skin, but it be somewhat dark; it is a rising of the burn-
ing, and the priest shall pronounce him clean: for it is an inflammation
of the burning” (Translation of Latin term inflammationem) [1]. Since
then, this primeval term has undergone explications. Cornelius Celsus,
a Roman encyclopedist, explained it as “redness and swelling with heat
and pain,” which was later refined by Rudolf Virchow by adding “loss of
function.” In 2007, Ferrero Miliani clarified that inflammation is a non-
specific immune response that develops as an answer to any type of in-
jury, and indicates accelerated blood flow, vasodilation, extravasation
of fluids, increased cellular metabolism, soluble mediator response,
cellular influx, and extravasation of fluids [2]. Currently, the medical
lexicon states that inflammation is a local or systemic reaction in tissue
generated due to internal or external stimuli in order to remove an in-
jurious agent to prevent further progression and repair tissue damage.
Injury in tissue and exposure to irritants or pathogens are assumed to be
the main reasons for this acute tissue or cellular process. Although un-
der normal conditions its reactions are circumscribed, it converts into
a chronic state upon prolonged exposure to inflammatory stimuli [2].
1.2 Causes and symptoms of inflammation
The skin is considered an immunological and mechanical bar-
rier that safeguards one’s body from the external environment.
Inflammation and Natural Products. https://doi.org/10.1016/B978-0-12-819218-4.00003-1
1
© 2021 Elsevier Inc. All rights reserved.
2 Chapter 1 Inflammation, symptoms, benefits, reaction, and biochemistry
However, any sort of damage to this shield opens a gateway for the
inflammation-causing agents to invade the body. These causative
agents are multifarious such as viral or bacterial pathogens; matter
such as metal parts, sharp objects, or foreign particles that enter tissue;
chemical agents such as radiation, alcohol, and autoimmunity; and
local tissue injury. These agents stimulate inflammation but are self-
limiting in the acute phase and turn chronic through the perpetual ex-
posure of these causative agents [2]. Generally, inflammation gives rise
to redness, heat, and swelling. However, there may be other noninflam-
matory causes for these symptoms. To illustrate, myositis and tendinitis
are often misunderstood with inflammation. Therefore, at the cellular
level, inflammation that arises due to the delay in the onset of muscular
sores, which consequently cause mild discomfort or tenderness upon
palpation, could be considered the cardinal signs of inflammation [3].
1.3 Types of inflammation
Inflammation developed in response to tissue injury or pathogens
can be subdivided into acute and chronic inflammation. The major
differences in acute and chronic inflammation are shown in Table 1.1.
Acute inflammation does not persist long and can be controlled with-
out even forming lesions. Chronic inflammation lasts for a longer
duration and is formed when the subject with acute inflammation is
continuously exposed to causative agents. Further, chronic inflamma-
tion is subdivided into primary chronic inflammation and secondary
chronic inflammation [2, 4].
Table 1.1 Difference between acute and chronic inflammation.
S. No. Inflammation Acute inflammation Chronic inflammation
1. Causative agents Injured tissue, pathogen Prolonged acute inflammation: autoimmune
reactions, nondegradable pathogen,
prolonged invasion of foreign bodies
2. Duration Couple of days Months or years
3. Onset Immediate Delayed
4. Major cells involved Mononuclear cells (macrophages, Mononuclear cells (fibroblast, macrophages,
monocytes), neutrophils monocytes, plasma cells, lymphocytes)
5. Primary mediators Eicosanoids, vasoactive amines Growth factors, hydrolytic enzymes, reactive
oxygen species, IFN-γ, cytokines
6. Outcomes Resolution, chronic inflammation, Fibrosis, tissue destruction
abscess formation
Chapter 1 Inflammation, symptoms, benefits, reaction, and biochemistry 3
1.3.1 Acute inflammation
The invasion by inflammation-causing agents or a nonself-
antigen stimulates the innate immune system and thereby the im-
mune responses. These are actuated mechanisms such as serotonin
and histamine release; escalation of vascular penetrability; chemo-
tactic factor secretion; and adhesion molecule hyperexpression on
endothelial cells [4]. It is identified as the expulsion of plasma pro-
teins and fluids with the simultaneous relocation of leukocytes, espe-
cially neutrophils, into the affected area [5]. Besides, the production
of antibodies facilitates the release of mediators to accelerate the
local reaction along with the continual intake of cells such as gran-
ulocytes, monocytes, lymphocytes, and plasma proteins from the
peripheral blood [4]. An acute inflammatory response is a defense
mechanism developed against the causative agents such as viruses,
bacteria, and parasites to facilitate wound repair. The chemical me-
diators produced commonly in acute inflammation are leukotrienes,
bradykinin, prostaglandin, histamine, anaphylotoxin, complement
system, and nitric oxide. To cease inflammation, the cyclooxygenase
(Cox) enzyme must be inhibited. It is the prime responsible factor
that converts arachidonic acid to prostaglandin H2, where prosta-
glandin H2 radically increases during inflammation [5]. Thus, this
process is temporary and exists until the inflammation-causing
agents are debarred [4].
1.3.2 Chronic inflammation
Chronic inflammation is also called nonresolving inflammation
or inflammaging, which is a dysregulatory, prolonged, and maladap-
tive response that produces constant active inflammation, followed
by tissue destruction and unsuccessful tissue repair. Moreover,
age-related inflammation occurs in a low and continuous way where
the escalated levels of proinflammatory cytokines and C-reactive
proteins (CRP) are activated and antiinflammatory cytokines are
reduced but asymptomatic with the level variation of pathophysi-
ological modification. Although the mechanism of chronic inflam-
mation is unknown, mitochondrial dysfunction, chronic inflection,
hormonal changes, redox stress, epigenetic damage, immunosenes-
cence, and glycation are suspected modes of action of this type of
inflammation [6]. This inexorable inflammation is an age-associated
disease that has a pernicious effect on the host cells as it fraternizes
with numerous pathogenic diseases such as cancer, rheumatoid ar-
thritis, coronary heart disease, obesity, inflammatory bowel disease,
atherosclerosis, Crohn’s disease, autoimmune diseases, diabetes,
and so on [5, 7]. It is further divided into primary and secondary
chronic inflammation.
4 Chapter 1 Inflammation, symptoms, benefits, reaction, and biochemistry
1.3.2.1 Primary chronic inflammation
In this category, the onset of inflammation projects a clear reaction
marked with increased permeability and vascularity as well as no or
minimal neutrophil infiltration. In addition, cell-mediated immune
responses are generated against the body cells that become prey to the
immune system. Primary chronic inflammation is associated with au-
toimmune diseases such as thyroiditis and certain tumors (exhibiting
lymphocytic infiltration) as well as rheumatoid arthritis (exhibiting T
and B mixed cells, neutrophils, and plasma cells).
1.3.2.2 Secondary chronic inflammation
This type of chronic inflammation occurs when acute inflamma-
tion persists due to the continuous exposure to causative agents that
converts the inflammatory lesions into chronic inflammation to ex-
pel polymorphonuclear cells and normalize endothelial activation,
vascular permeability, and vasodilation. The progression of inflam-
mation is suggestive of the infiltration of cells that are mainly mono-
nuclear in nature such as lymphocytes and monocyte-macrophage
series cells. Examples include a chronic infection such as tuberculosis
that forms sarcoidosis, chronic granulomas, and contact dermatitis;
human immunodeficiency virus (HIV); and cytomegalovirus (CMV)
[4]. Further, tissue immunity is the major local source as well as out-
lying inflammation that could be considered responsible for chronic
inflammation. Certain cases are related to the development of this
type of inflammation, even in the absence of pathogens. Helicobacter
pylori infection exemplifies such cases where the unwavering inflam-
mation eventually leads to cancer [8].
1.4 Benefits of inflammation
Inflammation is regarded as a necessary evil that makes the sur-
rounding immune cells aware of infection existing at any area. This in-
volvement of cellular pathways plays a vital role in regulating normal
cellular activities [5].
1.4.1 Inflammation as a necessary evil
The immune cells such as dendritic cells (DCs) and macrophages
liberate proinflammatory cytokines such as tumor necrosis factor-α
(TNF-α) and interferon gamma (IFN-γ) by combining the pattern
recognition receptors (PRRs) and pathogen-associated molecular
patterns (PAMPs) that exist on the surface of bacteria or on the DNA/
RNA of the viruses. Subsequently, the vasodilation of blood vessels oc-
curs due to the release of other chemicals that accelerate the intake of