Human RANTES (CCL5)
- Known as:
- Human RANTES (CCL5)
- Catalog number:
- GEM-300-180P20
- Product Quantity:
- 20 ug
- Category:
- -
- Supplier:
- SeraLab
- Gene target:
- Human RANTES (CCL5)
Related genes to: Human RANTES (CCL5)
- Gene:
- CCL5 NIH gene
- Name:
- C-C motif chemokine ligand 5
- Previous symbol:
- D17S136E, SCYA5
- Synonyms:
- RANTES, SISd, TCP228, MGC17164
- Chromosome:
- 17q12
- Locus Type:
- gene with protein product
- Date approved:
- 1990-07-05
- Date modifiied:
- 2016-03-01
Related products to: Human RANTES (CCL5)
Related articles to: Human RANTES (CCL5)
- Natural compounds with anti-inflammatory properties are increasingly explored as therapeutic agents due to their lower risk of side effects compared with conventional drugs. Fisetin, a dietary bioflavonol abundant in fruits and vegetables, exhibits anti-inflammatory activity in several cell types, including murine macrophages. However, its effects on human macrophages remain unclear. In this study, human pro-inflammatory M1 macrophages were generated from THP-1 monocytes using PMA, LPS, and IFN-γ. The effects of fisetin on cytokine and chemokine secretion, reactive oxygen species (ROS) production, apoptosis, and phagocytic activity were evaluated. In addition, the NF-κB, MAPK, and NLRP3 inflammasome pathways were analyzed. This study shows that fisetin pre-treatment significantly suppressed LPS/IFN-γ-induced secretion of pro-inflammatory cytokines (IL-6, TNF-α, IL-1β, IL-8) and chemokines (MCP-1, CCL5, CXCL9, CXCL10). It also reduced ROS generation, NLRP3 inflammasome activation, and phagocytic activity. Mechanistically, fisetin inhibited NF-κB activation as well as JNK/MAPK and p38/MAPK signaling, indicating that its anti-inflammatory actions are mediated through multiple pathways. Importantly, fisetin did not affect the viability or proliferation of THP-1-derived macrophages, suggesting that reduced cytokine release was primarily due to attenuation of macrophage polarization rather than cytotoxicity. Fisetin attenuates inflammatory responses in human M1 macrophages through suppression of NF-κB, MAPK, and NLRP3 inflammasome signaling. By limiting cytokine release, ROS production, and phagocytic activity without impairing cell survival, fisetin emerges as a promising natural candidate for managing chronic inflammatory disorders, including atherosclerosis, neurodegenerative diseases, and inflammatory bowel disease. - Source: PubMed
Onpan NattayaLorthongpanich ChanchaoKheolamai PakpoomChingsuwanrote PimjaiRodboon NapachaiLuanpitpong SudjitSaisawang ChontichaIssaragrisil Surapol - The aim of the present study was to elucidate the cellular and molecular mechanisms underlying refractory recurrent in-stent restenosis (RISR), thereby facilitating the identification of potential therapeutic targets. Coronary blood samples were obtained from culprit lesions of patients with RISR and non-ISR controls and subjected to single-cell RNA sequencing to comprehensively characterize immune cell heterogeneity and identify pathogenic signaling pathways. Key molecular mechanisms were validated in independent clinical samples using flow cytometry, monocyte-vascular smooth muscle cell (VSMC) coculture systems, and in vitro functional assays. Causality was further assessed using a monocyte-specific Fos knockdown mouse model of carotid wire injury to evaluate its role in vascular remodeling. Results revealed a pronounced inflammatory immune signature in RISR, with marked upregulation of activator protein-1 (AP-1) gene expression and transcriptional activity in monocytes as a central feature. Upstream mechanistic analyses identified the CCL5-CCR1/p38 MAPK axis as a key driver of AP-1 activation, promoting proinflammatory cytokine release and inducing a proliferative phenotypic switch in VSMCs. In vivo, monocyte-specific Fos knockdown significantly attenuated neointimal hyperplasia and luminal stenosis following vascular injury. Targeting monocyte AP-1 signaling may represent a novel therapeutic strategy for refractory restenosis driven by localized coronary inflammation. - Source: PubMed
Yu MiaoJiang YuHuang JiWei Zhi-YaoSong Zhi-FengTan Fang-ShunHuang Si-ZhuangYuan Jian-SongYe Shao-DongCui Jin-GangZhao Han-JunGao Li-JianYou Hong-ZhaoZeng YanYang Wei-XianQian Hai-Yan - Cheilitis is a lip-specific inflammatory disorder lacking safe long-term therapies. Topical glucocorticoids are limited by adverse effects, highlighting the need for plant-derived immunomodulators with dual anti-inflammatory and barrier-repairing effects. - Source: PubMed
Publication date: 2026/09/28
Zhu AnmingLiu JunxiCao XianxianWu JiahuiXiao FengkunLiu YouyunShen YanzhenWang FeifeiQu Liping - Postnatal choline supplementation improves memory, non-verbal IQ, executive function, and white-matter microstructure in children with fetal alcohol spectrum disorder (FASD) across randomized controlled trials; however, peripheral and brain biomarkers of these effects are uncharacterized. - Source: PubMed
Publication date: 2026/09/16
Tran Phu VMaxim Zia LEckerle Judith KZeisel Steven HGeorgieff Michael KWozniak Jeffrey R - Excessive inflammation is a critical contributor to impaired oral mucosal wound healing, yet effective therapeutic strategies are still lacking. Although dehydrocorydaline (DHC) has been reported to exhibit anti-inflammatory and analgesic properties, its role in wound healing and the underlying mechanisms have not been fully elucidated. This study aimed to investigate whether DHC accelerates palatal wound healing and to elucidate the role of the p38 mitogen-activated protein kinase (MAPK)/CCL2 signaling axis in DHC-mediated regulation of macrophage chemotaxis. , macrophages were stimulated with 1 μg/mL lipopolysaccharide (LPS) and treated with DHC at 0.1, 1, and 10 μM. The chemotactic response and inflammatory function of macrophages were assessed using real-time PCR, ELISA, Western blotting, and Transwell assays. Molecular docking simulations and Western blotting analyses were performed to examine the regulatory effect of DHC on MAPK signaling pathway. , a full-thickness palatal mucoperiosteal wound extending from the left maxillary first to third molars was established in mice by scalpel scraping. The effects of topical 10 μM DHC gel on wound healing were evaluated using stereomicroscopy, histological staining, and real-time PCR at 0, 3, and 5 days post-modeling. , DHC effectively downregulated the expression of chemokines, including C-C motif chemokine ligand 2 (), , , C-X-C motif chemokine ligand 10 (), and , with the most significant inhibitory effect on (70.8% inhibition). In Transwell assays, DHC reduced macrophage migration by 68.2%. Mechanistically, DHC prominently inhibited the activation of the MAPK signaling pathway. , DHC treatment accelerated wound healing and markedly reduced macrophage infiltration in mouse palatal wound tissues. These findings demonstrated that DHC accelerated palatal wound healing 1.6-fold in mice. DHC suppressed macrophage chemotaxis by 68.2% through modulation of the MAPK signaling pathway. - Source: PubMed
Publication date: 2026/08/27
Chen YingyiLiu ZhaonaWang YijiaXia GuiyangLiu YitongXia HuanWang MinfengLin ShengLiu Yi