Pyrogallol-Phloroglucinol-6,6-Bieckol Alleviates Obesity and Systemic Inflammation in a Mouse Model by Reducing Expression of RAGE and RAGE Ligands

Choi, Junwon; Oh, Seyeon; Son, Myeongjoo; Byun, Kyunghee

doi:10.3390/md17110612

Cited by 19 publications

(25 citation statements)

References 46 publications

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“…Several studies have shown that RAGE is related to obesity. Especially, the adipocytes of obese human show higher RAGE expression than those of the lean human [47] and accumulate RAGE ligands as well in the adipose tissues of HFD and obesity models [48][49][50]. In our study, ECE reduced TLR4, RAGE, and NF-κB expressions in the adipose tissues of HFD-fed mice (Figures 4(c) and 4(d)).…”

Section: Effects Of E Cava Extract On Tlr4 Rage and Nf-κbsupporting

confidence: 56%

The Phlorotannin-Rich Fraction ofEcklonia cavaExtract Attenuated the Expressions of the Markers Related with Inflammation and Leptin Resistance in Adipose Tissue

Son

Choi

et al. 2020

International Journal of Endocrinology

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Obesity is associated with systemic chronic inflammation, and it induces central leptin resistance which blocks the appetite-suppressing effect of leptin and leptin resistance in adipocytes. In the present study, we evaluated the effects of Ecklonia cava extract (ECE), which contained rich phlorotannins, on inflammation and leptin resistance in the adipose tissue of a diet-induced obese model. Effects of ECE on fat deposition, inflammation, M1/M2 macrophage, and T-cell infiltrations were investigated, and leptin resistance and SOCS3 were also measured in adipose tissue. Furthermore, ECE attenuated the expression of inflammation-related receptors such as TLR4 and RAGE and leptin resistance by reducing SOCS3 expression, increasing expression of leptin receptor in adipose tissue, and increasing lipolysis. ECE showed antiadiposity and anti-inflammatory effects, attenuated leptin resistance, and increased lipolysis in the diet-induced obese model. This study shows that ECE is a suitable dietary supplement candidate for the prevention or treatment of obesity or obesity-associated diseases, especially inflammation-related diseases.

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Section: Effects Of E Cava Extract On Tlr4 Rage and Nf-κbsupporting

confidence: 56%

The Phlorotannin-Rich Fraction ofEcklonia cavaExtract Attenuated the Expressions of the Markers Related with Inflammation and Leptin Resistance in Adipose Tissue

Son

Choi

et al. 2020

International Journal of Endocrinology

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“…Several studies have suggested that intracellular ROS generation can be increased by MGO; thus, this may play an important role in AGE-RAGE formation [45][46][47]. Furthermore, Deshpande et al reported the ROS-mediated proteolytic cleavage of procaspase-3 in the mitochondria of HUVECs [48].…”

Section: Discussionmentioning

confidence: 99%

Isosamidin from Peucedanum japonicum Roots Prevents Methylglyoxal-Induced Glucotoxicity in Human Umbilical Vein Endothelial Cells via Suppression of ROS-Mediated Bax/Bcl-2

Lee

Ahn

et al. 2020

Antioxidants

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Methylglyoxal (MGO) is a highly reactive metabolite of glucose. Elevated levels of MGO induce the generation of reactive oxygen species (ROS) and cause cell death in endothelial cells. Vascular endothelial cell damage by ROS has been implicated in the progression of diabetic vascular complications, cardiovascular diseases, and atherosclerosis. In this study, the protective effect of isosamidin, isolated from Peucedanum japonicum roots, on MGO-induced apoptosis was investigated using human umbilical vein endothelial cells (HUVECs). Among the 20 compounds isolated from P. japonicum, isosamidin showed the highest effectiveness in inhibiting MGO-induced apoptosis of HUVECs. Pretreatment of HUVECs with isosamidin significantly prevented the generation of ROS and cell death induced by MGO. Isosamidin prevented MGO-induced apoptosis in HUVECs by downregulating the expression of Bax and upregulating the expression of Bcl-2. MGO treatment activated mitogen-activated protein kinases (MAPKs), such as p38, c-Jun N terminal kinase (JNK), and extracellular signal-regulated kinase (ERK). In contrast, pretreatment with isosamidin strongly inhibited the activation of p38 and JNK. Furthermore, isosamidin caused the breakdown of the crosslinks of the MGO-derived advanced glycation end products (AGEs). These findings suggest that isosamidin from P. japonicum may be used as a preventive agent against MGO-mediated endothelial dysfunction in diabetes. However, further study of the therapeutic potential of isosamidin on endothelial dysfunction needs to explored in vivo models.

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“…Mice were fed different diets as described below and provided drinking water ad libitum for eight weeks. For the first four weeks, mice received either a regular normal fat diet (NFD) or a 45% HFD (Research Diet, USA) adapted from a previous study [ 36 ].…”

Section: Methodsmentioning

confidence: 99%

Pyrogallol-Phloroglucinol-6,6-Bieckolon Attenuates Vascular Smooth Muscle Cell Proliferation and Phenotype Switching in Hyperlipidemia through Modulation of Chemokine Receptor 5

Son

Park

et al. 2020

Marine Drugs

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Hyperlipidemia induces vascular smooth muscle cell (VSMC) proliferation and phenotype switching from contractile to synthetic. This process is involved in arterial remodeling via the chemokine ligand 5 (CCL5)/chemokine receptor 5 (CCR5) pathway. Arterial remodeling is related to atherosclerosis or intimal hyperplasia. The purpose of this study was to evaluate whether pyrogallol-phloroglucinol-6,6-bieckol (PPB) from E. cava reduces VSMC proliferation and phenotype switching via the CCL5/CCR5 pathway. The CCL5/CCR5 expression, VSMC proliferation and phenotypic alterations were evaluated using a cell model of VSMC exposed in hyperlipidemia, and an animal model of mice fed a high-fat-diet (HFD). The expression of CCL5/CCR5 increased in both the cell and animal models of hyperlipidemia. Treatment with PPB decreased CCL5/CCR5 expression in both models. The expression of contractile markers of VSMCs, including alpha-smooth muscle actin (α-SMA), smooth muscle myosin heavy chain (SM-MHC), and smooth muscle protein 22 alpha (SM22α), were decreased by hyperlipidemia and restored after treatment with PPB. The silencing of CCR5 attenuated the effects of PPB treatment. VSMC proliferation and the intima-media thickness of the aortas, increased with HFD and decreased after treatment with PPB. The VSMC proliferation ratio and messenger ribonucleic acid (mRNA) expression of cell cycle regulatory factors increased in the in vitro model and were restored after treatment with PPB. PPB treatment reduced VSMC proliferation and phenotype switching induced by hyperlipidemia through inhibition of the CCL5/CCR5 pathway.

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Pyrogallol-Phloroglucinol-6,6-Bieckol Alleviates Obesity and Systemic Inflammation in a Mouse Model by Reducing Expression of RAGE and RAGE Ligands

Cited by 19 publications

References 46 publications

The Phlorotannin-Rich Fraction ofEcklonia cavaExtract Attenuated the Expressions of the Markers Related with Inflammation and Leptin Resistance in Adipose Tissue

The Phlorotannin-Rich Fraction ofEcklonia cavaExtract Attenuated the Expressions of the Markers Related with Inflammation and Leptin Resistance in Adipose Tissue

Isosamidin from Peucedanum japonicum Roots Prevents Methylglyoxal-Induced Glucotoxicity in Human Umbilical Vein Endothelial Cells via Suppression of ROS-Mediated Bax/Bcl-2

Pyrogallol-Phloroglucinol-6,6-Bieckolon Attenuates Vascular Smooth Muscle Cell Proliferation and Phenotype Switching in Hyperlipidemia through Modulation of Chemokine Receptor 5

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