A New Compound Isolated from the Reduced Ribose–Tryptophan Maillard Reaction Products Exhibits Distinct Anti-inflammatory Activity

Qin, Dan; Li, Lin; Li, Jing; Li, Jinlong; Zhao, Di; Li, Yuting; Zhang, Xia

doi:10.1021/acs.jafc.8b01561

Cited by 18 publications

(5 citation statements)

References 53 publications

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“…For example, fructose-tyrosine MRPs were found to exhibit anti-inflammatory activity in astrocytes and BV-2 cells in cell experiments [57] . A compound, named BF-4, isolated from the products of the ribose-tryptophan Maillard reaction, reduced the levels of pro-inflammatory factors and inhibited nuclear transcription factor-κB (NF-κB) activation and mitogen-activated protein kinase (MAPK) phosphorylation through suppressing phosphorylation of IκBα, p65, p38 and c-Jun N-terminal kinase (JNK) to achieve its antiinflammatory activity [58] . There are many researchs on the cellular anti-inflammatory capacity of MRPs, and it is not worth describing them all.…”

Section: Anti-inflammatory Effectmentioning

confidence: 99%

Effects of Maillard reaction and its product AGEs on aging and age-related diseases

Peng¹,

Gao²,

Zeng³

et al. 2024

Food Science and Human Wellness

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Maillard reaction (MR) is a non-enzymatic browning reaction commonly seen in food processing, which occurs between reducing sugars and compounds with amino groups. Despite certain advantages based on Maillard reaction products (MRPs) found in some food for health and storage application have appeared, however, the MR occurring in human physiological environment can produce advanced glycation end products (AGEs) by non-enzymatic modifi cation of macromolecules such as proteins, lipids and nucleic acid, which could change the structure and functional activity of the molecules themselves. In this review, we take AGEs as our main object, on the one hand, discuss physiologic aging, that is, age-dependent covalent cross-linking and modifi cation of proteins such as collagen that occur in eyes and skin containing connective tissue. On the other hand, pathological aging associated with autoimmune and infl ammatory diseases, neurodegenerative diseases, diabetes and diabetic nephropathy, cardiovascular diseases and bone degenerative diseases have been mainly proposed. Based on the series of adverse effects of accelerated aging and disease pathologies caused by MRPs, the possible harm caused by some MR can be slowed down or inhibited by artifi cial drug intervention, dietary pattern and lifestyle control. It also stimulates people's curiosity to continue to explore the potential link between the MR and human aging and health, which should be paid more attention to for the development of life sciences.

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Section: Anti-inflammatory Effectmentioning

confidence: 99%

Effects of Maillard reaction and its product AGEs on aging and age-related diseases

Peng¹,

Gao²,

Zeng³

et al. 2024

Food Science and Human Wellness

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“…Consistent with a previous study, we found that G-Rg1 increased the phosphorylation of AMPK in HepG2 cells. AMPK is the main kinase regulator of its downstream genes ACC α , SREBP-1c, and FAS, which play a major role in adipocyte differentiation and lipid management [35]. In our study, it was shown that G-Rg1 suppressed the activity of ACC α , SREBP-1c, and FAS through the phosphorylation of AMPK (Figure 4).…”

Section: Discussionmentioning

confidence: 63%

Ginsenoside Rg1 Ameliorates Palmitic Acid-Induced Hepatic Steatosis and Inflammation in HepG2 Cells via the AMPK/NF-κB Pathway

Xiao

Zhang

Yang

et al. 2019

International Journal of Endocrinology

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Nonalcoholic fatty liver disease (NAFLD) is one of the common diseases in the world, and it can progress from simple lipid accumulation to sustained inflammation. The present study was designed to investigate the effects and underlying mechanisms of ginsenoside Rg1 (G-Rg1) treatment on NAFLD in vitro. HepG2 cells were treated with palmitic acid (PA) to induce steatosis and inflammation and then successively incubated with G-Rg1. Lipids accumulation was analyzed by Oil Red O staining and intracellular triglyceride (TG) quantification. Inflammatory conditions were examined by quantifying the levels of cell supernatant alanine transaminase/aspartate aminotransferase (ALT/AST) and secretory proinflammatory cytokines, including IL-1β, IL-6, and TNF-α in the cell supernatants. Quantitative RT-PCR and western blotting were used to measure the expressions of genes and proteins associated with lipogenic synthesis and inflammation, including AMP-activated protein kinase (AMPK) and nuclear factor-kappa B (NF-κB) pathways. HepG2 cells were pretreated with an AMPK inhibitor; then, Oil Red O staining and TG quantification were performed to study the lipid deposition. Phospho-AMPK (Thr172) (p-AMPK) and phospho-acetyl-CoA carboxylase (Ser79) (p-ACCα) were quantified by immunoblotting. Immunofluorescence was performed to demonstrate the nuclear translocation of NF-κB P65. The present study showed that PA markedly increased the intracellular lipid droplets accumulation and TG levels, but decreased AMPK phosphorylation and the expressions of its downstream lipogenic genes. However, G-Rg1 alleviated hepatic steatosis and reduced the intracellular TG content; these changes were accompanied by the activation of the AMPK pathway. In addition, blocking AMPK by using the AMPK inhibitor markedly abolished the G-Rg1-mediated protection against PA-induced lipid deposition in HepG2 cells. Furthermore, G-Rg1 reduced the ALT/AST levels and proinflammatory cytokines release, which were all enhanced by PA. These effects were correlated with the inactivation of the NF-κB pathway and translocation of P65 from the cytoplasm to the nucleus. Overall, these results suggest that G-Rg1 effectively ameliorates hepatic steatosis and inflammation, which might be associated with the AMPK/NF-κB pathway.

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“…IL-6 and TNF-α are two major important molecules involved in the response to foreign materials, and they are considered to be indicators of the degree of inflammation . Maintaining IL-6 and TNF-α at moderate levels is regarded as an effective treatment for tissue damage or inflammatory diseases …”

Section: Resultsmentioning

confidence: 99%

“…51 Maintaining IL-6 and TNF-α at moderate levels is regarded as an effective treatment for tissue damage or inflammatory diseases. 52 To obtain insights into the effects of CA, CGA, CA−Cys, and CGA−Cys on the LPS-induced inflammatory cytokine secretion in RAW 264.7 murine macrophage cells, the cytokine production of IL-6 and TNF-α was evaluated by ELISA (Figure 11). After 24 h of culture, LPS treatment significantly stimulated the production of inflammatory cytokines compared with the resting RAW 264.7 cells (P < 0.001), whereas all the compounds of CA, CGA, CA−Cys, and CGA−Cys significantly inhibited the production of IL-6 and TNF-α in LPStreated RAW 264.7 cells compared with the LPS group.…”

Section: ■ Results and Discussionmentioning

confidence: 99%

Phenolic Acid–Amino Acid Adducts Exert Distinct Immunomodulatory Effects in Macrophages Compared to Parent Phenolic Acids

Liu

Poojary

Zhu

et al. 2023

J. Agric. Food Chem.

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Caffeic acid (CA) and chlorogenic acid (CGA) are commonly found phenolic acids in plant-derived foods and beverages. Their corresponding adducts with cysteine (Cys) have been detected in coffee-containing beverages. However, despite the well-documented antioxidant and anti-inflammatory activity of CA and CGA, the immunomodulatory activities of the Cys adducts (CA–Cys and CGA–Cys) are unknown. The adducts were therefore synthesized, and their immunomodulatory effects were studied in lipopolysaccharide (LPS)-treated RAW 264.7 cells and compared to the activity of the parent phenolic acids. CA and CGA generally down-regulated the inflammatory responses. However, RNA-sequencing showed that the LPS-induced pathways related to Toll-like receptor signaling, chemokine signaling, and NOD-like receptor signaling, and JAK-STAT/MAPK signaling pathways were upregulated in adduct-treated cells relative to parent phenolic acids, while neurodegenerative disorder-related pathways and metabolic pathways were downregulated. Production of prostaglandin E2 (PGE2), interleukin-6, tumor necrosis factor-α (TNF-α), and reactive oxygen species (ROS) was all inhibited by CA and CGA (P < 0.05). PGE2 and TNF-α were further suppressed in adduct-stimulated cells (P < 0.05), but ROS production was increased. For example, TNF-α produced by 100 μM CGA-stimulated cells and 100 μM CGA–Cys adduct-stimulated cells were 4.46 ± 0.23 and 1.61 ± 0.18 ng/mL, respectively. Thus, the addition of the Cys moiety drastically alters the anti-inflammatory activity of phenolic compounds.

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A New Compound Isolated from the Reduced Ribose–Tryptophan Maillard Reaction Products Exhibits Distinct Anti-inflammatory Activity

Cited by 18 publications

References 53 publications

Effects of Maillard reaction and its product AGEs on aging and age-related diseases

Effects of Maillard reaction and its product AGEs on aging and age-related diseases

Ginsenoside Rg1 Ameliorates Palmitic Acid-Induced Hepatic Steatosis and Inflammation in HepG2 Cells via the AMPK/NF-κB Pathway

Phenolic Acid–Amino Acid Adducts Exert Distinct Immunomodulatory Effects in Macrophages Compared to Parent Phenolic Acids

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