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Bioactive Compounds and Chronic Inflammation

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A special issue of Nutrients (ISSN 2072-6643). This special issue belongs to the section "Phytochemicals and Human Health".

Deadline for manuscript submissions: closed (28 February 2021) | Viewed by 45329

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Dr. Francesca Oliviero

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Rheumatology Unit, Department of Medicine DIMED, University of Padova, 35128 Padova, Italy
Interests: pathogenetic mechanisms in crystal-induced inflammation; the role of calcium crystals in osteoarthritis; biomarkers in psoriatic arthritis; synovial fluid analysis; the influence of bioactive compounds in inflammation and crystal-induced arthritis; diet in rheumatic diseases
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Dear Colleagues,

Over the last ten years significant attention has been placed on the different beneficial properties of bioactive compounds. Their capacity to influence the inflammatory process and modulate the immune system has been widely documented by in vitro studies and experimental animal models. However, their role in human nutrition in relation to the development and progression of chronic inflammatory diseases has only recently been considered.

Chronic inflammatory diseases including autoimmune, metabolic, cardiovascular, pulmonary, neurodegenerative, hepatic, intestinal, and many other diseases, are a consequence of persistent inflammatory triggers, which cause a low-grade inflammatory status in the body. Among them, stress, smoking, infections, diet, dysbiosis, and obesity are the most investigated risk factors. Dysbiosis, in particular, has been strongly associated with chronic inflammation, raising the possibility to modulate chronic disease development and progression through microbiome manipulation.

Chronic inflammation represents an additional risk factor in developing comorbidities. There is, indeed, a clear interaction between chronic inflammation and development of cardiovascular diseases such as atherosclerosis, a process that is generally aggravated by pharmacological therapy.

In this context bioactive compounds might have a crucial role both in preventing the development of chronic inflammatory diseases and their comorbidities and modulating their clinical outcome.

The purpose of this Special Issue is to collect several original research articles and reviews dealing with health effects of bioactive compounds in relation to human nutrition.

Dr. Francesca Oliviero
Guest Editor

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Keywords

chronic inflammation
bioactive compounds
inflammatory molecular mechanisms
chronic inflammatory diseases
autoimmune diseases
metabolic syndrome
rheumatic diseases
obesity
cardiovascular diseases
inflammatory bowel disease

Published Papers (10 papers)

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Research

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13 pages, 4230 KiB

Open AccessArticle

Polydatin Prevents Calcium Pyrophosphate Crystal-Induced Arthritis in Mice

by Francesca Oliviero, Paola Galozzi, Anna Scanu, Francesca Galuppini, Vanni Lazzarin, Silvia Brocco, Giampietro Ravagnan, Paolo Sfriso, Roberta Ramonda, Paolo Spinella, Leonardo Punzi, Gianmaria Pennelli and Roberto Luisetto

Nutrients 2021, 13(3), 929; https://doi.org/10.3390/nu13030929 - 13 Mar 2021

Cited by 8 | Viewed by 2835

Abstract

Background: Polydatin is a stilbenoid with important antioxidant, anti-inflammatory, and immunomodulating properties. The aim of this study was to assess the anti-inflammatory preventive effect of polydatin in the mouse model of acute arthritis induced by calcium pyrophosphate (CPP) crystals. Methods: Acute arthritis was induced by the injection of a suspension of sterile CPP crystals into the ankle joint of Balb/c mice. Animals were randomized to receive polydatin or colchicine (the control drug) according to a prophylactic and a therapeutic protocol. The primary outcome was the variation of ankle swelling obtained after crystal injection and treatment, while histological parameters such as leukocyte infiltration, IL-1ß and CXCL1 levels and tissue expression were considered as secondary outcomes. Results: Prophylactic treatment with PD significantly diminished ankle swelling after 48 h from crystal injection. Secondary outcomes such as leukocyte infiltration, necrosis, edema, and synovitis were also decreased. PD caused a reduction in circulating levels of IL-1ß and CXCL1, as well as their tissue expression. By contrast, the therapeutic administration of PD did not have any beneficial effect. Conclusions: PD can effectively prevent acute inflammatory response to crystals in the mouse model of CPP crystal-induced arthritis. These results suggest that this bioactive compound might be used in the prevention of crystal-induced acute attacks in humans. Full article

(This article belongs to the Special Issue Bioactive Compounds and Chronic Inflammation)

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16 pages, 2595 KiB

Open AccessArticle

Pharmacokinetic Analysis of Carnosic Acid and Carnosol in Standardized Rosemary Extract and the Effect on the Disease Activity Index of DSS-Induced Colitis

by Jacob P. Veenstra, Bhaskar Vemu, Restituto Tocmo, Mirielle C. Nauman and Jeremy J. Johnson

Nutrients 2021, 13(3), 773; https://doi.org/10.3390/nu13030773 - 27 Feb 2021

Cited by 16 | Viewed by 3456

Abstract

Rosemary extract (RE) is an approved food preservative in the European Union and contains dietary phytochemicals that are beneficial for gastrointestinal health. This study investigated the effects of RE on dextran sodium sulfate (DSS)-induced colitis and also determined the pharmacokinetics of dietary phytochemicals administered to mice via oral gavage. Individual components of rosemary extract were separated and identified by LC–MS/MS. The pharmacokinetics of two major diterpenes from RE, carnosic acid (CA) and carnosol (CL), administered to mice via oral gavage were determined. Then, the effect of RE pre-treatment on the disease activity index (DAI) of DSS-induced colitis in mice was investigated. The study determined that 100 mg/kg RE significantly improved DAI in DSS-induced colitis compared to negative control. Sestrin 2 protein expression, which increased with DSS exposure, was reduced with RE treatment. Intestinal barrier integrity was also shown to improve via fluorescein isothiocyanate (FITC)–dextran administration and Western blot of zonula occludens-1 (ZO-1), a tight junction protein. Rosemary extract was able to improve the DAI of DSS-induced colitis in mice at a daily dose of 100 mg/kg and showed improvement in the intestinal barrier integrity. This study suggests that RE can be an effective preventative agent against IBD. Full article

(This article belongs to the Special Issue Bioactive Compounds and Chronic Inflammation)

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22 pages, 4873 KiB

Open AccessArticle

Protein Digests and Pure Peptides from Chia Seed Prevented Adipogenesis and Inflammation by Inhibiting PPARγ and NF-κB Pathways in 3T3L-1 Adipocytes

by Mariana Grancieri, Hércia Stampini Duarte Martino and Elvira Gonzalez de Mejia

Nutrients 2021, 13(1), 176; https://doi.org/10.3390/nu13010176 - 8 Jan 2021

Cited by 29 | Viewed by 4496

Abstract

The objective was to evaluate the mechanisms of digested total proteins (DTP), albumin, glutelin, and pure peptides from chia seed (Salvia hispanica L.) to prevent adipogenesis and its associated inflammation in 3T3-L1 adipocytes. Preadipocytes (3T3-L1) were treated during differentiation with either DTP or digested albumin or glutelin (1 mg/mL) or pure peptides NSPGPHDVALDQ and RMVLPEYELLYE (100 µM). Differentiated adipocytes also received DTP, digested albumin or glutelin (1 mg/mL), before (prevention) or after (inhibition) induced inflammation by addition of conditioned medium (CM) from inflamed macrophages. All treatments prevented adipogenesis, reducing more than 50% the expression of PPARγ and to a lesser extent lipoprotein lipase (LPL), fatty acid synthase (FAS), sterol regulatory element-binding protein 1 (SREBP1), lipase activity and triglycerides. Inflammation induced by CM was reduced mainly during prevention, while DTP decreased expression of NF-κB (−48.4%), inducible nitric oxide synthase (iNOS) (−46.2%) and COX-2 (−64.5%), p < 0.05. Secretions of nitric oxide, PGE2 and TNFα were reduced by all treatments, p < 0.05. DTP reduced expressions of iNOS (−52.1%) and COX-2 (−66.4%). Furthermore, digested samples and pure peptides prevented adipogenesis by modulating PPARγ and additionally, preventing and even inhibiting inflammation in adipocytes by inhibition of PPARγ and NF-κB expression. These results highlight the effectiveness of digested total proteins and peptides from chia seed against adipogenesis complications in vitro. Full article

(This article belongs to the Special Issue Bioactive Compounds and Chronic Inflammation)

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15 pages, 2581 KiB

Open AccessArticle

Oligo-Fucoidan Improves Diabetes-Induced Renal Fibrosis via Activation of Sirt-1, GLP-1R, and Nrf2/HO-1: An In Vitro and In Vivo Study

by Wen-Chun Yu, Ren-Yeong Huang and Tz-Chong Chou

Nutrients 2020, 12(10), 3068; https://doi.org/10.3390/nu12103068 - 8 Oct 2020

Cited by 41 | Viewed by 4567

Abstract

Fucoidan extracted from brown algae has multiple beneficial functions. In this study, we investigated the effects of low-molecular-weight fucoidan (oligo-FO) on renal fibrosis under in vitro and in vivo diabetic conditions, and its molecular mechanisms. Advanced glycation product (AGE)-stimulated rat renal proximal tubular epithelial cells (NRK-52E) and diabetic mice induced by high-fat diet and intraperitoneal injection of streptozotocin and nicotinamide were used. Oligo-FO treatment significantly inhibited anti-high mobility group box 1 (HMGB1)/RAGE/ anti-nuclear factor-kappa B (NF-κB)/transforming growth factor-β1 (TGF-β1)/TGF-β1R/Smad 2/3/fibronectin signaling pathway and HIF-1α activation in AGE-stimulated NRK-52E cells. Conversely, the expression and activity of Sirt-1; the levels of ubiquitin-specific peptidase 22 (USP22), p-AMPK, glucagon-like peptide-1 receptor (GLP-1R), and heme oxygenase-1 (HO-1); and Nrf2 activation were remarkably increased by oligo-FO in AGE-stimulated cells. However, the above effects of oligo-FO were greatly diminished by inhibiting Sirt-1, HO-1, or GLP-1R activity. Similar changes of these pro-fibrotic genes in the kidney and a marked attenuation of renal injury and dysfunction were observed in oligo-FO-treated diabetic mice. These findings indicated that the inhibitory effects of the oligo-FO on diabetes-evoked renal fibrosis are mediated by suppressing TGF-β1-activated pro-fibrogenic processes via Sirt-1, HO-1, and GLP-1R dependence. Collectively, fucoidan-containing foods or supplements may be potential agents for ameliorating renal diseases due to excessive fibrosis. Full article

(This article belongs to the Special Issue Bioactive Compounds and Chronic Inflammation)

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16 pages, 3532 KiB

Open AccessArticle

The Inhibitory Effect of Extra Virgin Olive Oil and Its Active Compound Oleocanthal on Prostaglandin-Induced Uterine Hypercontraction and Pain—Ex Vivo and In Vivo Study

by Yi-Fen Chiang, Hui-Chih Hung, Hsin-Yuan Chen, Ko-Chieh Huang, Po-Han Lin, Jen-Yun Chang, Tsui-Chin Huang and Shih-Min Hsia

Nutrients 2020, 12(10), 3012; https://doi.org/10.3390/nu12103012 - 30 Sep 2020

Cited by 21 | Viewed by 4212

Abstract

Primary dysmenorrhea is a common occurrence in adolescent women and is a type of chronic inflammation. Dysmenorrhea is due to an increase in oxidative stress, which increases cyclooxygenase-2 (COX-2) expression, increases the concentration of prostaglandin F2α (PGF2α), and increases the calcium concentration in uterine smooth muscle, causing excessive uterine contractions and pain. The polyphenolic compound oleocanthal (OC) in extra virgin olive oil (EVOO) has been shown to have an anti-inflammatory and antioxidant effect. This study aimed to investigate the inhibitory effect of extra virgin olive oil and its active ingredient oleocanthal (OC) on prostaglandin-induced uterine hyper-contraction, its antioxidant ability, and related mechanisms. We used force-displacement transducers to calculate uterine contraction in an ex vivo study. To analyze the analgesic effect, in an in vivo study, we used an acetic acid/oxytocin-induced mice writhing model and determined uterus contraction-related signaling protein expression. The active compound OC inhibited calcium/PGF2α-induced uterine hyper-contraction. In the acetic acid and oxytocin-induced mice writhing model, the intervention of the EVOO acetonitrile layer extraction inhibited pain by inhibiting oxidative stress and the phosphorylation of the protein kinase C (PKC)/extracellular signal-regulated kinases (ERK)/ myosin light chain (MLC) signaling pathway. These findings supported the idea that EVOO and its active ingredient, OC, can effectively decrease oxidative stress and PGF2α-induced uterine hyper-contraction, representing a further treatment for dysmenorrhea. Full article

(This article belongs to the Special Issue Bioactive Compounds and Chronic Inflammation)

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28 pages, 4607 KiB

Open AccessArticle

Nerolidol Mitigates Colonic Inflammation: An Experimental Study Using both In Vivo and In Vitro Models

by Vishnu Raj, Balaji Venkataraman, Saeeda Almarzooqi, Sanjana Chandran, Shreesh K. Ojha, Samir Attoub, Thomas E. Adrian and Sandeep B. Subramanya

Nutrients 2020, 12(7), 2032; https://doi.org/10.3390/nu12072032 - 8 Jul 2020

Cited by 14 | Viewed by 4034

Abstract

Nerolidol (NED) is a naturally occurring sesquiterpene alcohol present in various plants with potent anti-inflammatory effects. In the current study, we investigated NED as a putative anti-inflammatory compound in an experimental model of colonic inflammation. C57BL/6J male black mice (C57BL/6J) were administered 3% dextran sodium sulfate (DSS) in drinking water for 7 days to induce colitis. Six groups received either vehicle alone or DSS alone or DSS with oral NED (50, 100, and 150 mg/kg body weight/day by oral gavage) or DSS with sulfasalazine. Disease activity index (DAI), colonic histology, and biochemical parameters were measured. TNF-α-treated HT-29 cells were used as in vitro model of colonic inflammation to study NED (25 µM and 50 µM). NED significantly decreased the DAI and reduced the inflammation-associated changes in colon length as well as macroscopic and microscopic architecture of the colon. Changes in tissue Myeloperoxidase (MPO) concentrations, neutrophil and macrophage mRNA expression (CXCL2 and CCL2), and proinflammatory cytokine content (IL-1β, IL-6, and TNF-α) both at the protein and mRNA level were significantly reduced by NED. The increase in content of the proinflammatory enzymes, COX-2 and iNOS induced by DSS were also significantly inhibited by NED along with tissue nitrate levels. NED promoted Nrf2 nuclear translocation dose dependently. NED significantly increased antioxidant enzymes activity (Superoxide dismutase (SOD) and Catalase (CAT)), Hemeoxygenase-1 (HO-1), and SOD3 mRNA levels. NED treatment in TNF-α-challenged HT-29 cells significantly decreased proinflammatory chemokines (CXCL1, IL-8, CCL2) and COX-2 mRNA levels. NED supplementation attenuates colon inflammation through its potent antioxidant and anti-inflammatory activity both in in vivo and in vitro models of colonic inflammation. Full article

(This article belongs to the Special Issue Bioactive Compounds and Chronic Inflammation)

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14 pages, 3269 KiB

Open AccessArticle

L-Theanine Reduced the Development of Knee Osteoarthritis in Rats via Its Anti-Inflammation and Anti-Matrix Degradation Actions: In Vivo and In Vitro Study

by Hui Bai, Zhiheng Zhang, Yue Li, Xiaopeng Song, Tianwen Ma, Chunpeng Liu, Lin Liu, Rui Yuan, Xinyu Wang and Li Gao

Nutrients 2020, 12(7), 1988; https://doi.org/10.3390/nu12071988 - 3 Jul 2020

Cited by 29 | Viewed by 4794

Abstract

The etiology of osteoarthritis (OA) is multifactorial, with no effective disease-modifying-drugs. L-theanine has been reported to inhibit inflammatory responses in some diseases and this study aimed to investigate the effect of L-theanine on Interleukin-1(IL-1)β-stimulated chondrocytes, and in an injury-induced OA rat model. Primary chondrocytes were stimulated by IL-1β (10 ng/mL) for 24 h and then co-cultured with L-theanine for 24 h. The effects of L-theanine on IL-1β-stimulated expression of pro-inflammatory cytokines and hydrolytic enzyme were analyzed using Western blotting, quantitative polymerase chain reaction (q-PCR) and enzyme-linked immunosorbent assay (ELISA) kits. An immunofluorescence assay was used to detect nuclear factor kappa B (NF-κB) phosphorylation. OA was induced by anterior cruciate ligament transection (ACLT) surgery in rats and celecoxib was used as a positive control. OA severity was measured using the Osteoarthritis Research Society International (OARSI) grading system to describe histological changes. The results showed that L-theanine decreased the expression of pro-inflammatory mediators, including cyclooxygenase-2 (COX-2), prostaglandin E2 (PGE-2), inducible nitric oxide synthase (iNOS), and nitric oxide (NO), both in vivo and in vitro. L-theanine treatment inhibited IL-1β-induced upregulation of matrix metalloproteinases (MMP)-3 and MMP-13, as well as inhibited NF-κB p65 activation. In vivo animal model showed that L-theanine administration (200 mg/kg) significantly alleviated OA lesions and decreased OARSI score. Our data indicated that L-theanine decreased inflammatory cytokines and protected extracellular matrix degradation through inhibition of the NF-κB pathway, and L-theanine may be considered a promising therapeutic strategy in OA prevention. Full article

(This article belongs to the Special Issue Bioactive Compounds and Chronic Inflammation)

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11 pages, 2309 KiB

Open AccessArticle

Molecules from American Ginseng Suppress Colitis through Nuclear Factor Erythroid-2-Related Factor 2

by Anusha Chaparala, Hossam Tashkandi, Alexander A. Chumanevich, Erin E. Witalison, Anthony Windust, Taixing Cui, Mitzi Nagarkatti, Prakash Nagarkatti and Lorne J. Hofseth

Nutrients 2020, 12(6), 1850; https://doi.org/10.3390/nu12061850 - 21 Jun 2020

Cited by 13 | Viewed by 3309

Abstract

Ulcerative colitis (UC) is a chronic inflammatory bowel disease that affects millions of people worldwide and increases the risk of colorectal cancer (CRC) development. We have previously shown that American ginseng (AG) can treat colitis and prevent colon cancer in mice. We further fractionated AG and identified the most potent fraction, hexane fraction (HAG), and the most potent compound in this fraction, panaxynol (PA). Because (1) oxidative stress plays a significant role in the pathogenesis of colitis and associated CRC and (2) nuclear factor erythroid-2-related factor 2 (Nrf2) is the master regulator of antioxidant responses, we examined the role of Nrf2 as a mechanism by which AG suppresses colitis. Through a series of in vitro and in vivo Nrf2 knockout mouse experiments, we found that AG and its components activate the Nrf2 pathway and decrease the oxidative stress in macrophages (mΦ) and colon epithelial cells in vitro. Consistent with these in vitro results, the Nrf2 pathway is activated by AG and its components in vivo, and Nrf2^-/- mice are resistant to the suppressive effects of AG, HAG and PA on colitis. Results from this study establish Nrf2 as a mediator of AG and its components in the treatment of colitis. Full article

(This article belongs to the Special Issue Bioactive Compounds and Chronic Inflammation)

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24 pages, 4175 KiB

Open AccessArticle

Treatment of Non-Alcoholic Steatosis: Preclinical Study of a New Nutraceutical Multitarget Formulation

by Laura Micheli, Alessandra Pacini, Lorenzo Di Cesare Mannelli, Elena Trallori, Roberta D’Ambrosio, Carlo Bianchini, Pietro Lampertico and Carla Ghelardini

Nutrients 2020, 12(6), 1819; https://doi.org/10.3390/nu12061819 - 18 Jun 2020

Cited by 2 | Viewed by 3361

Abstract

Multifactorial pathogenesis of non-alcoholic steatohepatitis (NASH) disease, a wide-spread liver pathology associated with metabolic alterations triggered by hepatic steatosis, should be hit by multitarget therapeutics. We tested a multicomponent food supplement mixture (AP-NHm), whose components have anti-dislipidemic, antioxidant and anti-inflammatory effects, on in vitro and in vivo models of NASH. In vitro, hepatic cells cultures were treated for 24 h with 0.5 mM oleic acid (OA): in the co-treatment set cells were co-treated with AP-NH mixtures (AP-NHm, 1:3:10 ratio) and in the post-injury set AP-NHm was added for 48 h after OA damage. In vivo, C57BL/6 mice were fed with high-fat diet (HFD) for 12 weeks, inducing NASH at 7th week, and treated with AP-NHm at two dosages (1:3 ratio) in co-treatment or post-injury protocols, while a control group was fed with a standard diet. In in vitro co-treatment protocol, alterations of redox balance, proinflammatory cytokines release and glucose uptake were restored in a dose-dependent manner, at highest dosages also in post-injury regimen. In both regimens, pathologic dyslipidemias were also ameliorated by AP-NHm. In vivo, high-dose-AP-NHm-co-treated-HFD mice dose-dependently gained less body weight, were protected from dyslipidemia, and showed a lower liver weight. Dose-dependently, AP-NHm treatment lowered hepatic LDL, HDL, triglycerides levels and oxidative damage; co-treatment regimen was anti-inflammatory, reducing TNF-α and IL-8 levels. Hepatic lipidic infiltration significantly decreased in co-treated and post-injury-AP-NHm-HFD animals. The multitarget approach with AP-NHm was effective in preventing and reducing NASH-related pathologic features, warranting for the clinical development of this compound. Full article

(This article belongs to the Special Issue Bioactive Compounds and Chronic Inflammation)

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Review

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24 pages, 1407 KiB

Open AccessReview

Protective Effects of (E)-β-Caryophyllene (BCP) in Chronic Inflammation

by Rosaria Scandiffio, Federica Geddo, Erika Cottone, Giulia Querio, Susanna Antoniotti, Maria Pia Gallo, Massimo E. Maffei and Patrizia Bovolin

Nutrients 2020, 12(11), 3273; https://doi.org/10.3390/nu12113273 - 26 Oct 2020

Cited by 75 | Viewed by 9020

Abstract

(E)-β-caryophyllene (BCP) is a bicyclic sesquiterpene widely distributed in the plant kingdom, where it contributes a unique aroma to essential oils and has a pivotal role in the survival and evolution of higher plants. Recent studies provided evidence for protective roles of BCP in animal cells, highlighting its possible use as a novel therapeutic tool. Experimental results show the ability of BCP to reduce pro-inflammatory mediators such as tumor necrosis factor-alfa (TNF-α), interleukin-1β (IL-1β), interleukin-6 (IL-6), nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB), thus ameliorating chronic pathologies characterized by inflammation and oxidative stress, in particular metabolic and neurological diseases. Through the binding to CB2 cannabinoid receptors and the interaction with members of the family of peroxisome proliferator-activated receptors (PPARs), BCP shows beneficial effects on obesity, non-alcoholic fatty liver disease/nonalcoholic steatohepatitis (NAFLD/NASH) liver diseases, diabetes, cardiovascular diseases, pain and other nervous system disorders. This review describes the current knowledge on the biosynthesis and natural sources of BCP, and reviews its role and mechanisms of action in different inflammation-related metabolic and neurologic disorders. Full article

(This article belongs to the Special Issue Bioactive Compounds and Chronic Inflammation)

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