Bioactive Food as Dietary Interventions for Arthritis and Related Inflammatory Diseases
eBook - ePub

Bioactive Food as Dietary Interventions for Arthritis and Related Inflammatory Diseases

  1. 628 pages
  2. English
  3. ePUB (mobile friendly)
  4. Available on iOS & Android
eBook - ePub

Bioactive Food as Dietary Interventions for Arthritis and Related Inflammatory Diseases

About this book

Bioactive Food as Dietary Interventions for Arthritis and Inflammatory Diseases, Second Edition is a valuable scientific resource that focuses on the latest advances in bioactive food research and the potential benefit of bioactive food choice on arthritis. Written by experts from around the world, the book presents important information that can help improve the health of those at risk for arthritis and related conditions using food selection as its foundation.- Serves as a starting point for in-depth discussions in academic settings- Offers detailed, well-documented reviews outlining the ability of bioactive foods to improve and treat arthritis- Includes updated research on the global epidemic of diabetes- Updated with current research on antioxidant flavonoids, anti-Inflammatory natural foods, ginger and the effects of beef on inflammation- Documents foods that can affect metabolic syndrome and ways the associated information could be used to understand other diseases that share common etiological pathways

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Yes, you can access Bioactive Food as Dietary Interventions for Arthritis and Related Inflammatory Diseases by Ronald Ross Watson,Victor R Preedy,Victor R. Preedy in PDF and/or ePUB format, as well as other popular books in Biological Sciences & Nutrition, Dietics & Bariatrics. We have over one million books available in our catalogue for you to explore.
Section D
Nutraceuticals and Herbs in Modifications of Arthritis
Chapter 18

Role of Flavonoids in Management of Inflammatory Disorders

Rajesh Shukla; Vikas Pandey; Gautam P. Vadnere; Santram Lodhi Department of Pharmacy, Guru Ramdas Khalsa Institute of Science and Technology, Jabalpur, Madhya Pradesh, India
Department of Pharmacognosy, Smt. Sharadchandrika Suresh Patil College of Pharmacy, Chopda, Jalgaon, Maharashtra, India

Abstract

Flavonoids are a wide category of polyphenolic compounds that have a major role in the treatment of various inflammatory diseases, including arthritis, gastritis, nephritis, hepatitis, ulcerative colitis, Alzheimer's disease, atherosclerosis, and many allergic reactions. This chapter contains information about different flavonoids reported for the management of inflammatory disorders with their possible mechanism. These compounds also regulate the oxidative status and prevent damage caused by oxidative stress such as the antioxidant effect. The high levels of cytokines, such as tumor necrosis factor (TNF), interleukin (IL)-1, and IL-6, are allied with chronic inflammatory diseases. Some flavonoids, namely luteolin, quercetin, and apigenin, reduce cytokine expression and their secretion. It suggests that these flavonoids may have a therapeutic benefit in the treatment of inflammation-associated diseases as cytokine modulators. Flavonoids also have wide pharmacological effects by inhibiting some enzymes such as cyclooxygenase, aldose reductase, xanthenes oxidase, Ca2 + ATPase, phosphodiesterase, and lipoxygenase. In conclusion, flavonoids can produce health benefits in a variety of ways. This compilation work could be helpful to update current knowledge about different flavonoids and their effects, even at a molecular level, on inflammation and inflammatory-mediated diseases.

Keywords

Flavonoids; Antiinflammatory; Cytokines; Antioxidant; Oxidative stress
Abbreviations
AMPK adenosine 5′-monophosphate-activated protein kinase
AP-1 activating protein-1
CBG cytosolic β-glucosidase
COMTs catechol-O-methyltransferases
COXs cyclooxygenases
ELAM endothelial leukocyte adhesion molecule
ERK extracellular-signal-regulated kinases
GLUT glucose transporter 2
GST glutathione S-transferase
HO-1 heme oxygenase-1
HP-1 human monocytic cells
HUVECs human umbilical vein endothelial cells
IBD inflammatory bowel disease
ICAM intracellular adhesion molecule
IFN-γ interferon-γ
IKKb inhibitor of nuclear factor kappa-B kinase
IL interleukin
iNOS nitric oxide synthase
JNK c-Jun N-terminal kinase
LDL low density lipoproteins
LOX lipoxygenase
LPH lactase phloridzin hydrolase
LPS lipopolysaccharide
MAPK mitogen-activated protein kinase
MCP-1 monocyte chemotactic protein-1
MIP-2 macrophage-inflammatory protein-2
MMPs matrix metalloproteinases
NADPH nicotinamide adenine dinucleotide phosphate
NF-κB nuclear factor κ-light-chain-enhancer of activated B cells
NLRP3 nucleotide-binding oligomerization domain-like receptor family pyrin domain-containing 3 inflammasomes
NO nitric oxide
NOX NADPH oxidase
Nrf2 nuclear factor-erythroid 2 p45-related factor 2
PDGF platelet-derived growth factor
PMA phorbol-12-myristate-13-acetate
PMACI phorbol-12-myristate-13-acetate and calcium ionophore
PPAR peroxisome proliferator-activated receptor
PRDX2 peroxiredoxin-2
RA rheumatoid arthritis
ROS reactive oxygen species
SAPKs stress-activated protein kinases;
SGLT1 sodium dependent glucose transporter
SULTs sulfotransferases
TLR toll-like receptors
TNF tumor necrosis factor
TNFR tumor necrosis factor receptor
TRX thioredoxin
VCAM vascular cell adhesion molecule
VEGF vascular endothelial growth factor
ZnPP zinc protoporphyrin

1 Introduction

Inflammation is the state that results after activation of the immune system due to external attack or injury on the cells or tissues. The patient suffers from inflammation in any part of the body, and it is characterized by varied combinations of symptoms such as redness, tenderness, rash, burning, swelling, long-term soreness, and loss of function. It has been discovered that the onset of inflammation is a self-limiting and controlled process of the immune system.1 Releasing immune cells into the bloodstream is the integral part of the stages and processes of inflammation to the healing response in the body.
There are two types of inflammation that can occur: acute or chronic. In the case of acute inflammation, the immune system responds in a characteristic manner to infectious organisms or debris caused by injury, resulting in characteristic symptoms such as swelling, redness, pain, and heat. During such an acute inflammatory response, the body increases the level of leukocytes (i.e., granulocytes) in the affected tissue site. This process is followed by different steps that continue to involve the immune system until the injury or infection is back to homeostasis. This process usually takes from a few minutes to a number of hours.
Another type is chronic inflammation in which the degree of inflammation is elevated to weeks or months. Chronic inflammation is most likely due to the presence of foreign pathogens and continued production of inflammatory cytokines, or genetically driven autoimmune disease processes. During chronic inflammation, there is an increase in the biochemical markers of inflammation, such as excessive production of ROS, resulting in a state of oxidative stress and elevation of inflammatory cytokines (i.e., interferon-gamma (IFN-γ), IL-2, IL-4, IL-6, and IL-17).2
There are plentiful facts that certain proinflammatory cytokines such as IL-1β, IL-6, and TNF-α are concerned in the progression of pathological pain. IL-6 participates in an innermost role in the neuronal response to microglial, astrocytic activation, nerve injury, and in regulation of a neuronal neuropeptides phase.3 Another inflammatory cytokine is TNF-α, which acts as an entrenched, key function in a few pain models. Two major cell surface receptors through which TNF acts on several different signaling pathways are TNFR1 and TNFR2 for the regulation of NF-κB activation of inflammation and activation of stress-activated protein kinases (SAPKs) and apoptotic pathways. TNF-α plays an essential role in performing innate and adaptive immunity, proinflammatory properties, cell proliferation, and inflammatory and neuropathic hyperalgesia.4
Most drugs used to ease some inflammation-related indications pr...

Table of contents

  1. Cover image
  2. Title page
  3. Table of Contents
  4. Copyright
  5. Contributors
  6. Acknowledgments
  7. Section A: Overview and Background on Diet and Arthritis/Inflammation Modifications
  8. Section B: Nutrients and Inflammation Modification During Arthritis
  9. Section C: Foods in Arthritis
  10. Section D: Nutraceuticals and Herbs in Modifications of Arthritis
  11. Section E: Plants Extracts and Compounds in Arthritis
  12. Index