scholarly journals Nutraceutical Compounds Targeting Inflammasomes in Human Diseases

2020 ◽  
Vol 21 (14) ◽  
pp. 4829 ◽  
Author(s):  
Beatriz Castejón-Vega ◽  
Francesca Giampieri ◽  
José M. Alvarez-Suarez

The macromolecular complex known as “inflammasome” is defined as an intracellular multi-protein complex composed of a sensor receptor (PRR), an adaptor protein and an effector enzyme (caspase-1), which oligomerize when they sense danger, such as how the NLR family, AIM-2 and RIG-1 receptors protect the body against danger via cytokine secretion. Within the NLR members, NLRP3 is the most widely known and studied inflammasome and has been linked to many diseases. Nowadays, people’s interest in their lifestyles and nutritional habits is increasing, mainly due to the large number of diseases that seem to be related to both. The term “nutraceutical” has recently emerged as a hybrid term between “nutrition” and “pharmacological” and it refers to a wide range of bioactive compounds contained in food with relevant effects on human health. The relationship between these compounds and diseases based on inflammatory processes has been widely exposed and the compounds stand out as an alternative to the pathological consequences that inflammatory processes may have, beyond their defense and repair action. Against this backdrop, here we review the results of studies using several nutraceutical compounds in common diseases associated with the inflammation and activation of the NLRP3 inflammasomes complex. In general, it was found that there is a wide range of nutraceuticals with effects through different molecular pathways that affect the activation of the inflammasome complex, with positive effects mainly in cardiovascular, neurological diseases, cancer and type 2 diabetes.

2021 ◽  
Vol 22 (14) ◽  
pp. 7302
Author(s):  
Bryan Latrell Holloman ◽  
Mitzi Nagarkatti ◽  
Prakash Nagarkatti

Chronic inflammation is considered to be a silent killer because it is the underlying cause of a wide range of clinical disorders, from cardiovascular to neurological diseases, and from cancer to obesity. In addition, there are over 80 different types of debilitating autoimmune diseases for which there are no cure. Currently, the drugs that are available to suppress chronic inflammation are either ineffective or overtly suppress the inflammation, thereby causing increased susceptibility to infections and cancer. Thus, the development of a new class of drugs that can suppress chronic inflammation is imperative. Cannabinoids are a group of compounds produced in the body (endocannabinoids) or found in cannabis (phytocannabinoids) that act through cannabinoid receptors and various other receptors expressed widely in the brain and immune system. In the last decade, cannabinoids have been well established experimentally to mediate anti-inflammatory properties. Research has shown that they suppress inflammation through multiple pathways, including apoptosis and inducing immunosuppressive T regulatory cells (Tregs) and myeloid-derived suppressor cells (MDSCs). Interestingly, cannabinoids also mediate epigenetic alterations in genes that regulate inflammation. In the current review, we highlight how the epigenetic modulations caused by cannabinoids lead to the suppression of inflammation and help identify novel pathways that can be used to target autoimmune diseases.


2020 ◽  
Vol 10 (6) ◽  
pp. 411-429
Author(s):  
Ayman Khalil ◽  
Diana Tazeddinova

Abstract Polyphenols are a large family of more than 10,000 naturally occurring compounds, which exert countless pharmacological, biological and physiological benefits for human health including several chronic diseases such as cancer, diabetes, cardiovascular, and neurological diseases. Their role in traditional medicine, such as the use of a wide range of remedial herbs (thyme, oregano, rosemary, sage, mint, basil), has been well and long known for treating common respiratory problems and cold infections. This review reports on the most highlighted polyphenolic compounds present in up to date literature and their specific antiviral perceptive properties that might enhance the body immunity facing COVID-19, and other viral infectious diseases. In fact, several studies and clinical trials increasingly proved the role of polyphenols in controlling numerous human pathogens including SARS and MERS, which are quite similar to COVID-19 through the enhancement of host immune response against viral infections by different biological mechanisms. Thus, polyphenols ought to be considered as a potential and valuable source for designing new drugs that could be used effectively in the combat against COVID‐19 and other rigorous diseases.


2016 ◽  
Vol 36 (10) ◽  
pp. 1668-1685 ◽  
Author(s):  
Nikolett Lénárt ◽  
David Brough ◽  
Ádám Dénes

The role of inflammation in neurological disorders is increasingly recognised. Inflammatory processes are associated with the aetiology and clinical progression of migraine, psychiatric conditions, epilepsy, cerebrovascular diseases, dementia and neurodegeneration, such as seen in Alzheimer’s or Parkinson’s disease. Both central and systemic inflammatory actions have been linked with the development of brain diseases, suggesting that complex neuro-immune interactions could contribute to pathological changes in the brain across multiple temporal and spatial scales. However, the mechanisms through which inflammation impacts on neurological disease are improperly defined. To develop effective therapeutic approaches, it is imperative to understand how detrimental inflammatory processes could be blocked selectively, or controlled for prolonged periods, without compromising essential immune defence mechanisms. Increasing evidence indicates that common risk factors for brain disorders, such as atherosclerosis, diabetes, hypertension, obesity or infection involve the activation of NLRP3, NLRP1, NLRC4 or AIM2 inflammasomes, which are also associated with various neurological diseases. This review focuses on the mechanisms whereby inflammasomes, which integrate diverse inflammatory signals in response to pathogen-driven stimuli, tissue injury or metabolic alterations in multiple cell types and different organs of the body, could functionally link vascular- and neurological diseases and hence represent a promising therapeutic target.


2016 ◽  
Vol 44 (1) ◽  
pp. 293-298 ◽  
Author(s):  
Lucia E. Rameh ◽  
Jude T. Deeney

Type 2 diabetes is a complex disease. It results from a failure of the body to maintain energy homoeostasis. Multicellular organisms have evolved complex strategies to preserve a relatively stable internal nutrient environment, despite fluctuations in external nutrient availability. This complex strategy involves the co-ordinated responses of multiple organs to promote storage or mobilization of energy sources according to the availability of nutrients and cellular bioenergetics needs. The endocrine pancreas plays a central role in these processes by secreting insulin and glucagon. When this co-ordinated effort fails, hyperglycaemia and hyperlipidaemia develops, characterizing a state of metabolic imbalance and ultimately overt diabetes. Although diabetes is most likely a collection of diseases, scientists are starting to identify genetic components and environmental triggers. Genome-wide association studies revealed that by and large, gene variants associated with type 2 diabetes are implicated in pancreatic β-cell function, suggesting that the β-cell may be the weakest link in the chain of events that results in diabetes. Thus, it is critical to understand how environmental cues affect the β-cell. Phosphoinositides are important ‘decoders’ of environmental cues. As such, these lipids have been implicated in cellular responses to a wide range of growth factors, hormones, stress agents, nutrients and metabolites. Here we will review some of the well-established and potential new roles for phosphoinositides in β-cell function/dysfunction and discuss how our knowledge of phosphoinositide signalling could aid in the identification of potential strategies for treating or preventing type 2 diabetes.


2019 ◽  
Vol 21 (94) ◽  
pp. 92-96 ◽  
Author(s):  
Y. Y. Lavryshyn ◽  
B. V. Gutyj

The article presents the results of studies on the influence of cadmium load on the body of young cattle. The adverse effect of Cadmium on the liver causes a wide range of pathological changes at various levels of its organization. The purpose of the work was to investigate protein synthesize function on the liver of bulls for experimental chronic cadmium toxicity. The research was carried out on the basis of a farm at the village Ivanivtsi, Zhydachiv district of Lviv region, on 10 bulls of six months old, Ukrainian black-and-white milk breed, which were formed in 2 groups of 5 animals in each: control and experimental. Bulls of the control group were in the usual diet. Bulls of the experimental group were fed with forage with cadmium chloride at a dose of 0.04 mg/kg body weight of the animal. The research lasted for 30 days. Protein synthesize function of the liver was determined by the level of serum total protein and protein fractions. It was established that when feeding cows with feed of cadmium chloride in a dose of 0.04 mg/kg of body weight of an animal for 30 days in animals suppressed protein synthesize function of the liver, which manifests itself by lowering the total protein of blood. It reached the lowest level at the 20th day of the experiment, where, accordingly, it fluctuated within the limits of 61.9 ± 1.14 g/l. Reducing the level of total protein in the blood of the bulls of the experimental group under cadmium loading was due to lowering the level of albumin. At day 20 of the experiment, the level of albumin in the blood of animals in the experimental group decreased by 16.5%. On the background of general hypoproteinemia there is a significant imbalance between albumins and globulins in serum of diseased animals. It was established that the level of globulins increased in the blood of Bulls, which were under cadmium load. Increasing the level of globulins in blood serum of bulls reflects the intensity of inflammatory processes in their body for cadmium loading.


Open Medicine ◽  
2011 ◽  
Vol 6 (1) ◽  
pp. 1-10 ◽  
Author(s):  
Voja Pavlovic ◽  
M. Sarac

AbstractVitamin C (ascorbic acid) is an essential water-soluble nutrient that primarily exerts its effect on a host defense mechanisms and immune homeostasis and is the most important physiological antioxidant. Stable intake of vitamin C is essential for life in humans because the body does not synthesize it. Even the numerous studies have demonstrated that vitamin C supplementation stimulates the immune system, prevents DNA damage and significantly decreases the risk of a wide range of pathologies; the potential protective mechanisms are still largely unknown. This review summarizes the recently known facts about the role of vitamin C on the selected cells of the immune system and potential molecular mechanisms involved. Further, in this review, many new data about the positive effects of vitamin C on the immune system, potential toxicological effects, vitamin C supplementation in disease development, as well as some proposed mechanisms of vitamin C activity, are discussed.


2020 ◽  
Vol 134 (5) ◽  
pp. 547-570
Author(s):  
Miroslava Kacířová ◽  
Anna Zmeškalová ◽  
Lucia Kořínková ◽  
Blanka Železná ◽  
Jaroslav Kuneš ◽  
...  

Abstract Adipose tissue is an active metabolic organ that contributes to processes such as energy storage and utilization and to the production of a number of metabolic agents, such as adipokines, which play a role in inflammation. In this review, we try to elucidate the connections between peripheral inflammation at obesity and Type 2 diabetes and the central inflammatory process. Multiple lines of evidence highlight the importance of peripheral inflammation and its link to neuroinflammation, which can lead to neurodegenerative diseases such as dementia, Alzheimer’s disease (AD) and Parkinson’s disease. In addition to the accumulation of misfolded amyloid beta (Aβ) peptide and the formation of the neurofibrillary tangles of hyperphosphorylated tau protein in the brain, activated microglia and reactive astrocytes are the main indicators of AD progression. They were found close to Aβ plaques in the brains of both AD patients and rodent models of Alzheimer’s disease-like pathology. Cytokines are key players in pro- and anti-inflammatory processes and are also produced by microglia and astrocytes. The interplay of seemingly unrelated pathways between the periphery and the brain could, in fact, have a common denominator, with inflammation in general being a key factor affecting neuronal processes in the brain. An increased amount of white adipose tissue throughout the body seems to be an important player in pro-inflammatory processes. Nevertheless, other important factors should be studied to elucidate the pathological processes of and the relationship among obesity, Type 2 diabetes and neurodegenerative diseases.


2021 ◽  
Vol 14 ◽  
Author(s):  
Janelle E. Stanton ◽  
Sigita Malijauskaite ◽  
Kieran McGourty ◽  
Andreas M. Grabrucker

Metal dyshomeostasis plays a significant role in various neurological diseases such as Alzheimer’s disease, Parkinson’s disease, Autism Spectrum Disorders (ASD), and many more. Like studies investigating the proteome, transcriptome, epigenome, microbiome, etc., for years, metallomics studies have focused on data from their domain, i.e., trace metal composition, only. Still, few have considered the links between other “omes,” which may together result in an individual’s specific pathologies. In particular, ASD have been reported to have multitudes of possible causal effects. Metallomics data focusing on metal deficiencies and dyshomeostasis can be linked to functions of metalloenzymes, metal transporters, and transcription factors, thus affecting the proteome and transcriptome. Furthermore, recent studies in ASD have emphasized the gut-brain axis, with alterations in the microbiome being linked to changes in the metabolome and inflammatory processes. However, the microbiome and other “omes” are heavily influenced by the metallome. Thus, here, we will summarize the known implications of a changed metallome for other “omes” in the body in the context of “omics” studies in ASD. We will highlight possible connections and propose a model that may explain the so far independently reported pathologies in ASD.


2020 ◽  
Vol 11 (1) ◽  
pp. 7-10
Author(s):  
Khadiza Begum ◽  
Fahmida Islam ◽  
Farjana Aktar ◽  
Murshida Aziz ◽  
Tohfa E Ayub Tahiya

Background: In recent times much is talked about of serum ferritin, an acute phase reactant a marker of iron stores in the body and its association with diabetes mellitus. Studies implicate that increased body iron stores and subclinical hemochromatosis has been associated with the development of glucose intolerance, type 2 diabetes and its micro as well as macrovascular complications. Material & Methods: This study was carried out to examine and to observe for any relationship between serum ferritin with Type 2 diabetes mellitus. Our study populations were included 163. Among them 81 type 2 diabetes patients as a case (M=49,F=32, mean 44.68 age in years)and 82 normal healthy individual as a control ( M=35, F=47 , mean 34.71 in years). Results: Majority were healthy outpatients who had come for regular checkup and were matched with controls. Serum ferritin and FBS were estimated and other investigations. Results showed that although Serum ferritin was in the normal range value it was increased in type 2 diabetes patients than in controls and was statistically significant, we did get a positive correlation with duration of diabetes. It can be concluded that there were positive associations between serum ferritin and FBG, age, sex among study groups. Conclusion: In conclusion our study shows that there is significant correlation between increased serum ferritin in diabetes compared to individuals with normal blood sugars in this part and hyper ferritinemia may be one of the causes for development of insulin resistance before overt diabetes. Anwer Khan Modern Medical College Journal Vol. 11, No. 1: Jan 2020, P 7-10


2020 ◽  
Vol 2 (4) ◽  
pp. 14-31
Author(s):  
Élodie Dupey García

This article explores how the Nahua of late Postclassic Mesoamerica (1200–1521 CE) created living and material embodiments of their wind god constructed on the basis of sensory experiences that shaped their conception of this divinized meteorological phenomenon. In this process, they employed chromatic and design devices, based on a wide range of natural elements, to add several layers of meaning to the human, painted, and sculpted supports dressed in the god’s insignia. Through a comparative examination of pre-Columbian visual production—especially codices and sculptures—historical sources mainly written in Nahuatl during the viceregal period, and ethnographic data on indigenous communities in modern Mexico, my analysis targets the body paint and shell jewelry of the anthropomorphic “images” of the wind god, along with the Feathered Serpent and the monkey-inspired embodiments of the deity. This study identifies the centrality of other human senses beyond sight in the conception of the wind god and the making of its earthly manifestations. Constructing these deity “images” was tantamount to creating the wind because they were intended to be visual replicas of the wind’s natural behavior. At the same time, they referred to the identity and agency of the wind god in myths and rituals.


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