Protective Effect of the Natural Product, Chaetoglobosin K, on Lindane- and Dieldrin-induced Changes in Astroglia: Identification of Activated Signaling Pathways

2007 ◽  
Vol 25 (6) ◽  
pp. 1297-1308 ◽  
Author(s):  
Tatyana S. Sidorova ◽  
Diane F. Matesic
Keyword(s):  
Protective Effect ◽  
Signaling Pathways ◽  
Natural Product ◽  
Chaetoglobosin K ◽  
Induced Changes

scholarly journals Inhibitory Effect of LGS and ODE Isolated from the Twigs of Syringa oblata subsp. dilatata on RANKL-Induced Osteoclastogenesis in Macrophage Cells

Molecules ◽  
2021 ◽  
Vol 26 (6) ◽  
pp. 1779
Author(s):  
Ga-Ram Kim ◽  
Eun-Nam Kim ◽  
Kyoung Jin Park ◽  
Ki Hyun Kim ◽  
Gil-Saeng Jeong
Keyword(s):  
Protein Kinase ◽  
Bone Resorption ◽  
Signaling Pathways ◽  
Natural Product ◽  
Osteoclast Differentiation ◽  
Bone Diseases ◽  
Pivotal Role ◽  
Nuclear Factor ◽  
Bone Homeostasis ◽  
Nuclear Factor Kappa

Osteoblasts and osteoclasts play a pivotal role in maintaining bone homeostasis, of which excessive bone resorption by osteoclasts can cause osteoporosis and various bone diseases. However, current osteoporosis treatments have many side effects, and research on new treatments that can replace these treatments is ongoing. Therefore, in this study, the roles of ligustroside (LGS) and oleoside dimethylester (ODE), a natural product-derived compound isolated from Syringa oblata subsp. dilatata as a novel, natural product-derived osteoporosis treatments were investigated. In the results of this study, LGS and ODE inhibited the differentiation of receptor activator of nuclear factor kappa-Β ligand (RANKL)-induced RAW264.7 cells into osteoclasts without cytotoxicity, and down-regulated the activity of TRAP, a specific biomarker of osteoclasts. In addition, it inhibited bone resorption and actin ring formation, which are important functions and features of osteoclasts. Also, the effects of LGS and ODE on the mitogen-activated protein kinase (MAPK) and nuclear factor kappa-light-chain-enhancer of activated B (NF-κB) and phosphoinositide 3-kinases (PI3K)/ protein kinase B (Akt)/mechanistic target of rapamycin (mTOR) signaling pathways that play important roles in osteoclast differentiation were evaluated. In the results, LGS and ODE downregulated the phosphorylation of RANKL-induced MAPK and PI3K/Akt/mTOR proteins in a concentration-dependent manner, translocation of NF-κB into the nucleus was inhibited. As a result, the compounds LGS and ODE isolated from S. oblate subsp. dilatata effectively regulated the differentiation of RANKL-induced osteoclasts and inhibited the phosphorylation of signaling pathways that play a pivotal role in osteoclast differentiation. Therefore, these results suggest the possibility of LGS and ODE as new natural product treatments for bone diseases caused by excessive osteoclasts.

scholarly journals Protective Effect of Sulfated Polysaccharides from Celluclast-Assisted Extract of Hizikia fusiforme Against Ultraviolet B-Induced Skin Damage by Regulating NF-κB, AP-1, and MAPKs Signaling Pathways In Vitro in Human Dermal Fibroblasts

Marine Drugs ◽  
2018 ◽  
Vol 16 (7) ◽  
pp. 239 ◽  
Author(s):  
Lei Wang ◽  
WonWoo Lee ◽  
Jae Oh ◽  
Yong Cui ◽  
BoMi Ryu ◽  
...  
Keyword(s):  
Protective Effect ◽  
Signaling Pathways ◽  
Dermal Fibroblasts ◽  
Sulfated Polysaccharides ◽  
Dependent Manner ◽  
Human Dermal Fibroblasts ◽  
Skin Damage ◽  
Hizikia Fusiforme ◽  
Hdf Cells

Our previous study evaluated the antioxidant activities of sulfated polysaccharides from Celluclast-assisted extract of Hizikia fusiforme (HFPS) in vitro in Vero cells and in vivo in zebrafish. The results showed that HFPS possesses strong antioxidant activity and suggested the potential photo-protective activities of HFPS. Hence, in the present study, we investigated the protective effects of HFPS against ultraviolet (UV) B-induced skin damage in vitro in human dermal fibroblasts (HDF cells). The results indicate that HFPS significantly reduced intracellular reactive oxygen species (ROS) level and improved the viability of UVB-irradiated HDF cells in a dose-dependent manner. Furthermore, HFPS significantly inhibited intracellular collagenase and elastase activities, remarkably protected collagen synthesis, and reduced matrix metalloproteinases (MMPs) expression by regulating nuclear factor kappa B (NF-κB), activator protein 1 (AP-1), and mitogen-activated protein kinases (MAPKs) signaling pathways in UVB-irradiated HDF cells. These results suggest that HFPS possesses strong UV protective effect, and can be a potential ingredient in the pharmaceutical and cosmetic industries.

scholarly journals Detection of Treatment-Induced Changes in Signaling Pathways in Gastrointestinal Stromal Tumors Using Transcriptomic Data

2009 ◽  
Vol 69 (23) ◽  
pp. 9125-9132 ◽  
Author(s):  
Michael F. Ochs ◽  
Lori Rink ◽  
Chi Tarn ◽  
Sarah Mburu ◽  
Takahiro Taguchi ◽  
...  
Keyword(s):  
Signaling Pathways ◽  
Gastrointestinal Stromal Tumors ◽  
Stromal Tumors ◽  
Transcriptomic Data ◽  
Induced Changes

Abstract 489: Differential Phosphoproteomic Analysis of Platelet Activation by Specific Oxidized Phospholipids and Thrombin Reveals Mechanisms of Platelet Activation in Hyperlipidemia

2013 ◽  
Vol 33 (suppl_1) ◽  
Author(s):  
Alejandro Zimman ◽  
Bjoern Titz ◽  
Evangelia Komisopoulou ◽  
Thomas G Graeber ◽  
Eugene A Podrez
Keyword(s):  
Signaling Pathways ◽  
Signaling Pathway ◽  
Platelet Activation ◽  
Scavenger Receptor ◽  
Human Platelets ◽  
Oxidized Phospholipids ◽  
Systematic Analysis ◽  
Bioinformatic Tools ◽  
Induced Changes

We previously showed that specific oxidized phospholipids (oxPC CD36 ) activate platelets via the scavenger receptor CD36 and promote platelet hyper-reactivity in hyperlipidemia, however the signaling pathway(s) induced in platelets by oxPC CD36 are not defined. We employed mass spectrometry-based phosphoproteomics for the unbiased analysis of changes in protein phosphorylation induced by oxPC CD36 and thrombin, a strong platelet agonist, in human platelets. oxPC CD36 induced changes in phosphorylation of 148 unique phosphorylation sites (116 proteins) while thrombin induced changes of 297 unique sites (181 proteins). Most of the changes in phosphorylation induced by oxPC CD36 and thrombin identified in our study have never been reported before in platelets and include high- and low-abundant proteins with diverse molecular functions located in the plasma membrane, cytosol, or cytoskeleton. Analysis using multiple bioinformatic tools identified protein interaction networks, signaling pathways, activated kinases, and enriched phosphorylation motifs. Comparison between platelet agonists revealed multiple differences including the specific activation of a signaling pathway involving Src-family kinases (SFK), SYK kinase, and PLCγ2 by oxPC CD36 . Subsequent biochemical studies in human platelets demonstrated that this pathway is critical for platelet activation by oxPC CD36 and is downstream of CD36. In conclusion, systematic analysis of platelet activation pathways provided novel insights into the mechanism of platelet activation and specific signaling pathways induced by oxidized phospholipids that modulate platelet function in vivo in hyperlipidemia.

scholarly journals Resolvin D1 Alleviates Ventilator-Induced Lung Injury in Mice by Activating PPARγ/NF-κB Signaling Pathway

2019 ◽  
Vol 2019 ◽  
pp. 1-9 ◽  
Author(s):  
Haifa Xia ◽  
Jingxu Wang ◽  
Shujun Sun ◽  
Fuquan Wang ◽  
Yiyi Yang ◽  
...  
Keyword(s):  
Lung Injury ◽  
Protective Effect ◽  
Tidal Volume ◽  
Signaling Pathways ◽  
Lung Tissue ◽  
Fatty Acid Derivative ◽  
High Tidal Volume ◽  
Treatment Modalities ◽  
Resolvin D1 ◽  
Ventilator Induced Lung Injury

As one of the basic treatment modalities in the intensive care unit (ICU), mechanical ventilation can cause or aggravate acute lung injury or ventilator-induced lung injury (VILI). Resolvin D1 (RvD1) is an endogenous polyunsaturated fatty acid derivative with strong anti-inflammatory action. In this study, we explored if RvD1 possesses a protective effect on VILI. Mice were ventilated with high tidal volume (40 mL/kg, HVT) for 4 h and were then intraperitoneally administered RvD1 at the beginning of high tidal volume ventilation and given GW9662 (a PPAR-γ antagonist) intraperitoneally 30 min before ventilation. RvD1 attenuated VILI, as evidenced by improved oxygenation and reduced histological injury, compared with HVT -induced lung injury. Similarly, it could ameliorate neutrophil accumulation and production of proinflammatory cytokines in lung tissue. In contrast, the protective effect of RvD1 on lung tissue could be reversed by GW9662. RvD1 mitigated VILI by activating peroxisome proliferator-activated receptor gamma (PPAR-γ) and inhibiting nuclear factor-kappa B (NF-κB) signaling pathways in mice. In conclusion, RvD1 could reduce the inflammatory response in VILI by activating PPAR-γ and inhibiting NF-κB signaling pathways.

scholarly journals Protocatechuic Aldehyde Attenuates UVA-induced Photoaging in Human Dermal Fibroblast Cells by Suppressing MAPKs/AP-1 and NF-κB Signaling Pathways

2020 ◽  
Vol 21 (13) ◽  
pp. 4619
Author(s):  
Yuling Ding ◽  
Chanipa Jiratchayamaethasakul ◽  
Seung-Hong Lee
Keyword(s):  
Nitric Oxide ◽  
Protective Effect ◽  
Signaling Pathways ◽  
Inflammatory Responses ◽  
Dermal Fibroblast ◽  
Human Dermal Fibroblast ◽  
Potential Candidate ◽  
Ros Scavenging ◽  
Protocatechuic Aldehyde ◽  
Hdf Cells

Ultraviolet radiation (UV) is a major causative factor of DNA damage, inflammatory responses, reactive oxygen species (ROS) generation and a turnover of various cutaneous lesions resulting in skin photoaging. The purpose of this study is to investigate the protective effect of protocatechuic aldehyde (PA), which is a nature-derived compound, against UVA-induced photoaging by using human dermal fibroblast (HDF) cells. In this study, our results indicated that PA significantly reduced the levels of intracellular ROS, nitric oxide (NO), and prostaglandins-E2 (PGE2) in UVA-irradiated HDF cells. It also inhibited the levels of cyclooxygenase-2 (COX-2) and inducible nitric oxide synthase (iNOS) expression. Besides, PA significantly suppressed the expression of matrix metalloproteinases-1 (MMP-1) and pro-inflammatory cytokines and promoted collagen synthesis in the UVA-irradiated HDF cells. These events occurred through the regulation of activator protein 1 (AP-1), nuclear factor-κB (NF-κB), and p38 signaling pathways in UVA-irradiated HDF cells. Our findings suggest that PA enhances the protective effect of UVA-irradiated photoaging, which is associated with ROS scavenging, anti-wrinkle, and anti-inflammatory activities. Therefore, PA can be a potential candidate for the provision of a protective effect against UVA-stimulated photoaging in the pharmaceutical and cosmeceutical industries.

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