SOCS3
- Known as:
- SOCS3
- Catalog number:
- 11-406-C025
- Product Quantity:
- 0.025 mg
- Category:
- -
- Supplier:
- Exbio
- Gene target:
- SOCS3
Related genes to: SOCS3
- Gene:
- SOCS3 NIH gene
- Name:
- suppressor of cytokine signaling 3
- Previous symbol:
- -
- Synonyms:
- SSI-3, CIS3, SOCS-3, Cish3
- Chromosome:
- 17q25.3
- Locus Type:
- gene with protein product
- Date approved:
- 2002-11-13
- Date modifiied:
- 2019-04-23
Related products to: SOCS3
Related articles to: SOCS3
- This study aimed to investigate the mechanism of dihydroartemisinin(DHA) in ameliorating multiple sclerosis(MS). Hematoxylin and eosin(HE) staining was used to assess inflammatory cell infiltration, while luxol fast blue(LFB) staining and electron microscopy were performed to evaluate myelin sheath structure. In cell experiments, this study measured programmed cell death ligand 1(PD-L1) expression on BV2 cells and forkhead box protein p3(Foxp3) expression in Jurkat T cells co-cultured with BV2 cells, determined the C-C motif chemokine ligand 5(CCL5) concentration in the supernatant of BV2 cells, and evaluated BV2 cell chemotaxis. Western blot(WB) was performed to detect protein levels of receptor tyrosine kinase(AXL), phosphorylated AXL(p-AXL), signal transducer and activator of transcription 1(STAT1), phosphorylated STAT1(p-STAT1), and suppressors of cytokine signaling 3(SOCS3). To confirm the role of AXL, key cellular assays were repeated following inhibition of AXL. Additionally, under physiological conditions, the effects of DHA on body weight, spleen weight, and peripheral blood immune cell profiles were examined. The results showed that DHA significantly reduced disease scores, attenuated body weight loss, suppressed inflammatory infiltration, and promoted myelin sheath repair in experimental autoimmune encephalomyelitis(EAE) mice. At the cellular level, DHA upregulated PD-L1 expression on BV2 cells and Foxp3 expression in co-cultured Jurkat cells, and inhibited CCL5 release and BV2 cell chemotaxis. It also upregulated AXL, p-AXL, p-STAT1, and SOCS3 protein expression in BV2 cells. When AXL was inhibited, these effects are nullified. In healthy mice, DHA did not have any effect on their various parameters. In conclusion, DHA maintains inflammatory homeostasis in the EAE model by activating the AXL signaling pathway in microglia. - Source: PubMed
Zhang YangRan Qing-SenHan Jia-YinLiu LiDU Xin-KeWu Jing-WenYang QingChen YingWeng Xiao-GangZhu Xiao-XinLi Qi - Ulcerative colitis (UC) is a refractory inflammatory bowel disease characterized by gut microbiota dysbiosis and mucosal barrier disruption. Sarcandra glabra (Sg), a traditional herbal tea and dietary supplement, has been widely used to alleviate intestinal inflammation; however, its gut microbiota-dependent mechanism remains insufficiently clarified. In this study, Sg at 2, 4, and 8 g/kg was found to dose-dependently mitigate dextran sulfate sodium (DSS)-induced colitis in mice, restore mucosal barrier integrity by upregulating tight junction proteins and enhancing mucin secretion, and reduce serum levels of IL-1β, TNF-α, and IL-6. Integrative analysis of full-length 16S rRNA gene sequencing, transcriptomics, and metabolomics data revealed that Sg reshaped gut microbiota, selectively enriching Ligilactobacillus animalis while depleting Escherichia coli and Proteus vulgaris. We identified 8 microbiota-derived metabolites correlated with Ligilactobacillus animalis abundance, among which 2,3-dihydroxybenzoic acid (2,3-DHBA) exhibited the strongest protective effect against DSS-induced NCM460 cell damage. Mechanistic studies indicated that 2,3-DHBA effectively inhibited the IL-6/SOCS3 pathway and restored tight junction protein expression, effects that were reversed by exogenous IL-6. These findings demonstrate that Sg enriches for Ligilactobacillus animalis and its metabolite 2,3-DHBA, which suppresses IL-6-driven inflammation and repairs mucosal damage, supporting its potential as a microbiome-targeted dietary adjunct for UC. - Source: PubMed
Publication date: 2026/07/01
Huang ShaoweiChi XiaomeiSong SitingGao XinyiYu DedianHuang WenbinWang JiayiChen LixiaLi Hua - Spinal cord injury (SCI) leads to irreversible neurological deficits primarily through secondary injury mechanisms, including oxidative stress and glial dysfunction. Sulforaphane (SFN), a naturally occurring isothiocyanate, has shown antioxidant and anti-inflammatory effects in various neurological models, but its impact on Janus kinase/signal transducer and activator of transcription (JAK/STAT) signaling and microglial polarization in SCI remains unclear. Adult male Wistar rats were randomly assigned to Sham, SCI, or SCI + SFN groups (n = 10/group). SCI was induced by a moderate T10 contusion, and SFN (50 mg/kg, i.p.) was administered at 10 min, 72 h, and 7 days post-injury. Locomotor recovery was assessed using the Basso-Beattie-Bresnahan (BBB) scale. At day 14, spinal cord tissue was analyzed for oxidative stress markers, including reactive oxygen species (ROS), malondialdehyde (MDA), superoxide dismutase (SOD), and reduced glutathione (GSH), as well as JAK2/STAT3 signaling and microglial polarization. SCI significantly increased ROS and MDA levels while reducing SOD activity and GSH content. Phosphorylation of JAK2 and STAT3, along with glial fibrillary acidic protein (GFAP), tumor necrosis factor-α (TNF-α), and interleukin-6 (IL-6), was markedly elevated. SFN treatment restored antioxidant defenses, suppressed JAK2/STAT3 activation, partially recovered suppressor of cytokine signaling 3 (SOCS3), and reduced pro-inflammatory responses. Moreover, SFN shifted microglial polarization from a pro-inflammatory (M1) toward a reparative (M2) phenotype and significantly improved BBB locomotor scores compared with untreated SCI rats. SFN confers neuroprotection in SCI by reducing oxidative stress, modulating JAK/STAT signaling, rebalancing microglial polarization, and improving locomotor recovery. These findings highlight SFN as a promising candidate for therapeutic development in SCI. - Source: PubMed
Publication date: 2026/05/28
Saeed Zainab HameedWeshel Widyan GataaLafta Ali HusseinAmeen Murtadha AzeezAbbass Zainab HannonAkhtam AkramovAxmedov Shamshod - Incomplete thermal ablation (iTA) for hepatocellular carcinoma (HCC) fosters an immunosuppressive microenvironment driving local recurrence, yet the metabolic cues linking tissue injury to immune evasion remain undefined. Bile acids, particularly lithocholic acid (LCA), are elevated post-ablation, but their functional role in HCC recurrence is unknown. Here, we investigate whether LCA accumulation after iTA promotes tumor recurrence by suppressing antitumor immunity and identify the underlying molecular mechanism. - Source: PubMed
Publication date: 2026/06/28
Li RumeiLuo WanrongLi ZhaoxiZheng SuiLuo ManWei QiuxiaZhu XiaotongZhang WenyueLuo Baoming - In this Bioinformatics study, we took in account the cell types variation of tumor microenvironment (TME) in Pancreatic Ductal Adenocarcinoma (PDAC), with a particular attention to miRNAs dysregulated pathways influencing immune responses, and especially memory CD4+ T cells. - Source: PubMed
Publication date: 2026/05/22
Al-Janaby Mohammed SalihMannoush Salah HAl-Janabi Saif SSuleiman Ahmed AbdulJabbarAbdulkareem Ali HazimAlalwani Anmar KamilFahad Mustafa M