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Molecular, Genetic, and Biochemical Nutrition Commons

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Human and Clinical Nutrition

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NLRP3 inflammasome

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Articles 1 - 3 of 3

Full-Text Articles in Molecular, Genetic, and Biochemical Nutrition

Therapeutic Potential Of Garlic Chive-Derived Vesicle-Like Nanoparticles In Nlrp3 Inflammasome-Mediated Inflammatory Diseases, Baolong Liu, Xingzhi Li, Han Yu, Xuan Shi, You Zhou, Sophie Alvarez, Michael J. Naldrett, Stephen D. Kachman, Seung-Hyun Ro, Xinghui Sun, Soonkyu Chung, Lili Jing, Jiujiu Yu Sep 2021

Therapeutic Potential Of Garlic Chive-Derived Vesicle-Like Nanoparticles In Nlrp3 Inflammasome-Mediated Inflammatory Diseases, Baolong Liu, Xingzhi Li, Han Yu, Xuan Shi, You Zhou, Sophie Alvarez, Michael J. Naldrett, Stephen D. Kachman, Seung-Hyun Ro, Xinghui Sun, Soonkyu Chung, Lili Jing, Jiujiu Yu

Department of Nutrition and Health Sciences: Faculty Publications

Aberrant activation of the nucleotide-binding domain and leucine-rich repeat related (NLR) family, pyrin domain containing 3 (NLRP3) inflammasome drives the development of many complex inflammatory diseases, such as obesity, Alzheimer’s disease, and atherosclerosis. However, no medications specifically targeting the NLRP3 inflammasome have become clinically available. Therefore, we aim to identify new inhibitors of the NLRP3 inflammasome in this study. Methods: Vesicle-like nanoparticles (VLNs) were extracted from garlic chives and other Allium vegetables and their effects on the NLRP3 inflammasome were evaluated in primary macrophages. After garlic chive-derived VLNs (GC-VLNs) were found to exhibit potent anti-NLRP3 inflammasome activity in cell culture, …


Identification Of Anti-Inflammatory Vesicle-Like Nanoparticles In Honey, Xingyi Chen, Boalong Liu, Xingzhi Li, Thuy T. An, You Zhou, Gang Li, Judy Wu-Smart, Sophie Alvarez, Michael J. Naldrett, James Eudy, Gregory Kubik, Richard A. Wilson, Stephen D. Kachman, Juan Cui, Jiujiu Yu Jan 2021

Identification Of Anti-Inflammatory Vesicle-Like Nanoparticles In Honey, Xingyi Chen, Boalong Liu, Xingzhi Li, Thuy T. An, You Zhou, Gang Li, Judy Wu-Smart, Sophie Alvarez, Michael J. Naldrett, James Eudy, Gregory Kubik, Richard A. Wilson, Stephen D. Kachman, Juan Cui, Jiujiu Yu

Department of Nutrition and Health Sciences: Faculty Publications

Honey has been used as a nutrient, an ointment, and a medicine worldwide for many centuries. Modern research has demonstrated that honey has many medicinal properties, reflected in its anti-microbial, anti-oxidant, and anti-inflammatory bioactivities. Honey is composed of sugars, water and a myriad of minor components, including minerals, vitamins, proteins and polyphenols. Here, we report a new bioactive component‒vesicle-like nanoparticles‒in honey (H-VLNs). These HVLNs are membrane-bound nano-scale particles that contain lipids, proteins and small-sized RNAs. The presence of plant-originated plasma transmembrane proteins and plasma membrane-associated proteins suggests the potential vesicle-like nature of these particles. H-VLNs impede the formation and activation …


Inhibitory Effects Of Toll-Like Receptor 4, Nlrp3 Inflammasome, And Interleukin-1Β On White Adipocyte Browning, Meshail Okla, Walid Zaher, Musaad Alfayez, Soonkyu Chung Jan 2018

Inhibitory Effects Of Toll-Like Receptor 4, Nlrp3 Inflammasome, And Interleukin-1Β On White Adipocyte Browning, Meshail Okla, Walid Zaher, Musaad Alfayez, Soonkyu Chung

Department of Nutrition and Health Sciences: Faculty Publications

Adipose tissue expansion is accompanied by infiltration and accumulation of pro-inflammatory macrophages, which links obesity to pathologic conditions such as type 2 diabetes. However, little is known regarding the role of pro-inflammatory adipose tissue remodeling in the thermogenic activation of brown/beige fat. Here, we investigated the effect of pattern recognition receptors (PRR) activation in macrophages, especially the toll-like receptor 4 (TLR4) and Nod-like receptor 3 (NLRP3), on white adipocyte browning. We report that TLR4 activation by lipopolysaccharide repressed white adipocyte browning in response to β3-adrenergic receptor activation and caused ROS production and mitochondrial dysfunction, while genetic deletion of TLR4 protected …