Trans-10-hydroxy-2-decenoic acid protects against LPS-induced neuroinflammation through FOXO1-mediated activation of autophagy

You, Mengmeng; Miao, Zhuoning; Tian, Jing; Hu, Fuliang

doi:10.1007/s00394-019-02128-9

Cited by 23 publications

(31 citation statements)

References 43 publications

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“…The molecular events involved in the effect of bee products on catabolic genes and anabolic resistance in skeletal muscle could be much related to their hypoglycemic effects, which positively affect the quality of skeletal muscle. Evidence signifies a positive effect of royal jelly acid (10-HDA) on inflammation and autophagy via upregulation of AMPK, which subsequently alters NF-κB and NLRP3 inflammasome-IL1β signaling [ 129 ]. Positive effects of whole royal jelly on skeletal muscle are associated with improved insulin signaling [ 96 , 100 ].…”

Section: Mechanisms Of Action Of Royal Jelly Bee Pollen and Propmentioning

confidence: 99%

Apitherapy for Age-Related Skeletal Muscle Dysfunction (Sarcopenia): A Review on the Effects of Royal Jelly, Propolis, and Bee Pollen

Ali

Kunugi

2020

Foods

119

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The global pandemic of sarcopenia, skeletal muscle loss and weakness, which prevails in up to 50% of older adults is increasing worldwide due to the expansion of aging populations. It is now striking young and midlife adults as well because of sedentary lifestyle and increased intake of unhealthy food (e.g., western diet). The lockdown measures and economic turndown associated with the current outbreak of Coronavirus Disease 2019 (COVID-19) are likely to increase the prevalence of sarcopenia by promoting sedentarism and unhealthy patterns of eating. Sarcopenia has multiple detrimental effects including falls, hospitalization, disability, and institutionalization. Although a few pharmacological agents (e.g., bimagrumab, sarconeos, and exercise mimetics) are being explored in different stages of trials, not a single drug has been approved for sarcopenia treatment. Hence, research has focused on testing the effect of nutraceuticals, such as bee products, as safe treatments to prevent and/or treat sarcopenia. Royal jelly, propolis, and bee pollen are common bee products that are rich in highly potent antioxidants such as flavonoids, phenols, and amino acids. These products, in order, stimulate larval development into queen bees, promote defenses of the bee hive against microbial and environmental threats, and increase royal jelly production by nurse bees. Thanks to their versatile pharmacological activities (e.g., anti-aging, anti-inflammatory, anticarcinogenic, antimicrobial, etc.), these products have been used to treat multiple chronic conditions that predispose to muscle wasting such as hypertension, diabetes mellitus, cardiovascular disorder, and cancer, to name a few. They were also used in some evolving studies to treat sarcopenia in laboratory animals and, to a limited degree, in humans. However, a collective understanding of the effect and mechanism of action of these products in skeletal muscle is not well-developed. Therefore, this review examines the literature for possible effects of royal jelly, bee pollen, and propolis on skeletal muscle in aged experimental models, muscle cell cultures, and humans. Collectively, data from reviewed studies denote varying levels of positive effects of bee products on muscle mass, strength, and function. The likely underlying mechanisms include amelioration of inflammation and oxidative damages, promotion of metabolic regulation, enhancement of satellite stem cell responsiveness, improvement of muscular blood supply, inhibition of catabolic genes, and promotion of peripheral neuronal regeneration. This review offers suggestions for other mechanisms to be explored and provides guidance for future trials investigating the effects of bee products among people with sarcopenia.

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Section: Mechanisms Of Action Of Royal Jelly Bee Pollen and Propmentioning

confidence: 99%

Apitherapy for Age-Related Skeletal Muscle Dysfunction (Sarcopenia): A Review on the Effects of Royal Jelly, Propolis, and Bee Pollen

Ali

Kunugi

2020

Foods

119

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“…RJ protected LPS-stimulated BV-2 microglia against oxidative stress and attenuated microglial inflammatory processes that contribute to amyloidgenesis. It significantly decreased the production of ROS, NOS, IL-6, IL-1β, and TNF-α and increased the mRNA expression of antioxidants such as heme oxygenase-1 (HO-1) and glutathione peroxidase (GSH-Px) [ 113 , 114 ]. The major fatty acid in RJ, 10-HDA, protected the BBB against LPS-induced leakage by inhibiting the degradation of tight junction proteins (occludin, claudin-5 and ZO-1) in LPS-stimulated C57BL/6 mice, as well as by increasing the expression of tight junction proteins, and decreasing the expression of chemokines (CCL-2 and CCL-3), adhesion molecules (e.g., intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1)), and matrix metalloproteinases (MMP-2 and MMP-9) in LPS-stimulated human brain microvascular endothelial cells (HBMECs) [ 114 ].…”

Section: Effect Of Royal Jelly On Cognitive Performance and Relatementioning

confidence: 99%

“…In this context, positive effects of RJ (e.g., suppression of inflammation and oxidative stress, increased autophagy, etc.) have been associated with the activation of AMPK [ 114 ]. AMPK is an energy sensing pathway that gets activated under conditions that entail deficiency of cellular nutrients.…”

Section: Mechanisms Underlying Effects Of Rj On Cognition and Ad-rmentioning

confidence: 99%

“…Neuroinflammation broadens neuron loss by accelerating oxidative stress. A number of investigations included in this article challenged microglia or rodent models with LPS to induce a neuroinflammatory phenotype that was parallel to that in AD [ 113 , 114 , 117 ]. LPS induces inflammation by regulating the activity of NF-κB, MAPK, signal transducer and activator of transcription 1 (STAT1), and activator protein (AP-1), and c-Jun NH2-terminal kinases (JNK) [ 113 ].…”

Section: Mechanisms Underlying Effects Of Rj On Cognition and Ad-rmentioning

confidence: 99%

“…LPS induces inflammation by regulating the activity of NF-κB, MAPK, signal transducer and activator of transcription 1 (STAT1), and activator protein (AP-1), and c-Jun NH2-terminal kinases (JNK) [ 113 ]. Furthermore, markers of neuroinflammation are evidently high in AD models produced by toxic treatments [ 113 , 114 , 117 , 119 ]. In these experiments, RJ demonstrated anti-inflammatory effects by inhibiting the expression of proinflammatory cytokines (IL-6, IL-1β, and TNF-α) [ 113 , 114 , 117 , 119 ], chemokines (CCL-2, CCL-3) [ 114 ], and related genes of iNOS and cyclooxygenase-2 (COX-2) [ 113 ].…”

Section: Mechanisms Underlying Effects Of Rj On Cognition and Ad-rmentioning

confidence: 99%

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Royal Jelly as an Intelligent Anti-Aging Agent—A Focus on Cognitive Aging and Alzheimer’s Disease: A Review

Ali

2020

Antioxidants

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The astronomical increase of the world’s aged population is associated with the increased prevalence of neurodegenerative diseases, heightened disability, and extremely high costs of care. Alzheimer’s Disease (AD) is a widespread, age-related, multifactorial neurodegenerative disease that has enormous social and financial drawbacks worldwide. The unsatisfactory outcomes of available AD pharmacotherapy necessitate the search for alternative natural resources that can target various the underlying mechanisms of AD pathology and reduce disease occurrence and/or progression. Royal jelly (RJ) is the main food of bee queens; it contributes to their fertility, long lifespan, and memory performance. It represents a potent nutraceutical with various pharmacological properties, and has been used in a number of preclinical studies to target AD and age-related cognitive deterioration. To understand the mechanisms through which RJ affects cognitive performance both in natural aging and AD, we reviewed the literature, elaborating on the metabolic, molecular, and cellular mechanisms that mediate its anti-AD effects. Preclinical findings revealed that RJ acts as a multidomain cognitive enhancer that can restore cognitive performance in aged and AD models. It promotes brain cell survival and function by targeting multiple adversities in the neuronal microenvironment such as inflammation, oxidative stress, mitochondrial alterations, impaired proteostasis, amyloid-β toxicity, Ca excitotoxicity, and bioenergetic challenges. Human trials using RJ in AD are limited in quantity and quality. Here, the limitations of RJ-based treatment strategies are discussed, and directions for future studies examining the effect of RJ in cognitively impaired subjects are noted.

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Trans‑10‑Hydroxy‑2‐Decenoic Acid Alleviates Dextran Sulfate Sodium‐Induced Colitis in Mice via Regulating the Inflammasome‐Mediated Pyroptotic Pathway and Enhancing Colonic Barrier Function

Huang

Tao

Zhou

et al. 2022

Molecular Nutrition Food Res

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Scope The objective of this study is to explore the effects of 10‐hydroxy‐2‐decenoic acid (10‐HDA), the major fatty acid in royal jelly, on dextran sodium sulfate (DSS)‐induced mice ulcerative colitis (UC) and its potential mechanism of action. Methods and results Forty male C57BL/6 mice are randomly divided into five experimental groups: control, DSS, DSS + 25 (or 100)mg kg−1 d−1 10‐HDA, and DSS + 200 mg kg−1 d−1 mesalazine (ME). UC is induced in mice using 2.5% DSS in drinking water for 7 days. During the induction, these UC mice are orally administrated 10‐HDA or ME per day. Meanwhile, lipopolysaccharide (LPS)/adenosine‐triphosphate (ATP)‐stimulated THP1 cells are used as a model to test the effects of 10‐HDA. 10‐HDA reduces DSS‐induced pathological damage, reactive oxygen species (ROS) accumulation, neutrophil infiltration, and cytokine production in colonic tissue. Compared with the DSS group, the expressions of thioredoxin interacting protein (TXNIP), NOD‐like receptor family pyrin domain containing 3 (NLRP3), apoptosis‐associated speck‐like protein containing a caspase‐recruitment domain (ASC), cysteinyl aspartate specific proteinase‐1 (Caspase‐1), gasdermin‐D (GSDMD), N‐terminal domain of gasdermin‐D (N‐GSDMD), interleukin‐1β (IL‐1β), and interleukin‐18 (IL‐18) in the colon are decreased after administration of 10‐HDA. 10‐HDA also elevates the barrier integrity and the expressions of zonula occludens‐1 (ZO‐1) and Occludin in colonic epithelium exposed to DSS. In THP1 cells, the inflammasome‐mediated pyroptosis induced by LPS/ATP is inhibited by 10‐HDA pretreatment. Conclusion 10‐HDA alleviates DSS‐induced colitis by regulating the NLRP3 inflammasome‐mediated pyroptotic pathway and enhancing colonic barrier function.

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Trans-10-hydroxy-2-decenoic acid protects against LPS-induced neuroinflammation through FOXO1-mediated activation of autophagy

Cited by 23 publications

References 43 publications

Apitherapy for Age-Related Skeletal Muscle Dysfunction (Sarcopenia): A Review on the Effects of Royal Jelly, Propolis, and Bee Pollen

Apitherapy for Age-Related Skeletal Muscle Dysfunction (Sarcopenia): A Review on the Effects of Royal Jelly, Propolis, and Bee Pollen

Royal Jelly as an Intelligent Anti-Aging Agent—A Focus on Cognitive Aging and Alzheimer’s Disease: A Review

Trans‑10‑Hydroxy‑2‐Decenoic Acid Alleviates Dextran Sulfate Sodium‐Induced Colitis in Mice via Regulating the Inflammasome‐Mediated Pyroptotic Pathway and Enhancing Colonic Barrier Function

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