Ask about this productRelated genes to: IDO1 antibody
- Gene:
- IDO1 NIH gene
- Name:
- indoleamine 2,3-dioxygenase 1
- Previous symbol:
- IDO, INDO
- Synonyms:
- -
- Chromosome:
- 8p11.21
- Locus Type:
- gene with protein product
- Date approved:
- 1993-05-26
- Date modifiied:
- 2016-01-15
Related products to: IDO1 antibody
Related articles to: IDO1 antibody
- High-fat diets (HFD) are implicated in metabolic disorders through mechanisms involving hyperuricemia, gut dysbiosis, and intestinal barrier dysfunction. This study investigated the effects of pharmacological uric acid reduction on gut homeostasis in HFD-fed mice. We assessed serum uric acid, gut microbial composition, pro- and anti-inflammatory cytokine expression, intestinal barrier dysfunction markers, and tryptophan metabolism in mice subjected to HFD with or without allopurinol treatment. AhR antagonist CH-223191 was used to provide functional evidence for the role of AhR activation in mediating the observed effects. HFD induced hyperuricemia, microbial dysbiosis characterized by increased Proteobacteria and altered Firmicutes/Bacteroidetes ratios, and elevated pro-inflammatory cytokines (IL-1β, IL-6, TNF-α). These changes correlated with decreased IL-10 and IL-22, increased serum LPS, and systemic inflammation (IL-6, CRP). Allopurinol treatment normalized uric acid levels, restored microbial balance, reduced gut and systemic inflammation, improved intestinal barrier function, and modulated tryptophan metabolism by decreasing IDO1 activity and restoring indole production. Pharmacological blockade of AhR with CH-223191 reversed the anti-inflammatory and barrier-protective effects of allopurinol treatment, providing functional evidence for the role of AhR/IL22 axis in mediating gut protection. Targeting hyperuricemia effectively reverses HFD-induced gut dysbiosis, inflammation, and barrier dysfunction through metabolite-mediated immunoregulatory mechanisms involving the AhR-IL-22 axis. These findings propose uric acid modulation as a promising therapeutic strategy for metabolic and inflammatory gut diseases. - Source: PubMed
Publication date: 2026/09/04
Bouquez SoledadCampos Paola LópezOttobre MacarenaDuhalde-Vega Maite - To explore the processing synergistic effect of Rehmanniae Radix processed with Stephaniae Tetrandrae Radix juice on antidepressant efficacy, and to preliminarily investigate its underlying mechanism focusing on indoleamine 2,3-dioxygenase 1(IDO1). After preparation of Rehmanniae Radix processed with Stephaniae Tetrandrae Radix juice, a mouse model of depression was established using the chronic unpredictable mild stress(CUMS) paradigm. The conventional behavioral tests including sucrose preference test(SPT), tail suspension test(TST) and forced swimming test(FST) were performed, combined with pathological observation of the hippocampus by hematoxylin-eosin(HE) staining, to comprehensively evaluate the processing synergistic effect of Rehmanniae Radix processed with Stephaniae Tetrandrae Radix juice. Western blot(WB) and enzyme-linked immunosorbent assay(ELISA) were adopted to detect and analyze the hippocampal IDO1 protein expression level, as well as the levels of quinolinic acid(QUIN), representative inflammatory cytokines and neurotransmitters, thereby preliminarily exploring the mechanism of action. The results showed that the CUMS model induced a significant decrease in sucrose preference of mice in SPT(P<0.01), a significant increase in immobility time in TST and FST(P<0.01), as well as disordered arrangement, pyknosis and hyperchromasia.Moreover, the hippocampal IDO1 protein expression level was significantly up-regulated(P<0.01), and the QUIN content was significantly increased(P<0.01). The levels of pro-inflammatory cytokines tumor necrosis factor-α(TNF-α), interleukin-6(IL-6) and IL-17 were significantly increased(P<0.01), the level of anti-inflammatory cytokine IL-10 was significantly decreased(P<0.01), and the levels of monoamine neurotransmitters 5-hydroxytryptamine(5-HT), dopamine(DA) and norepinephrine(NE) were all significantly reduced(P<0.01). After the administration of crude Rehmanniae Radix and its processed products with Stephaniae Tetrandrae Radix juice at different processing juice ratios(10%, 15%, and 20%), all the above abnormal indicators induced by CUMS were significantly improved(P<0.05 or P<0.01). Notably, the processed product with 20% Stephaniae Tetrandrae Radix juice showed a significantly better improvement effect on the above indicators than the crude drug(P<0.01). This study demonstrates that the processed product of Rehmanniae Radix with Stephaniae Tetrandrae Radix juice can significantly enhance the antidepressant efficacy of Rehmanniae Radix, with the 20% ratio being the optimal one. The mechanism underlying its processing synergistic effect involves the down-regulation of hippocampal IDO1 protein expression, the reduction of QUIN production, resultant inhibition of neuroinflammation, and the elevation of monoamine neurotransmitter levels. - Source: PubMed
DU Chen-JieWang Jun-MingWu Xiao-HuiHe Qing-WenYang Dan - Tertiary lymphoid structures (TLS) are spatially organized immune niches associated with therapeutic response and favorable outcomes in breast cancer (BC). However, TLS assessment currently relies on invasive tissue-based analyses, and the biological mechanisms underlying imaging-based TLS prediction remain poorly understood. - Source: PubMed
Publication date: 2026/09/03
Yu YushuaiWang QingLin YidanHuang KaiyanWang RuijuanWang JunxiaoHuang XieweiZhang JieChen WeiweiChen RuiliangChen XuejunMeng FanZhang HengyuYuan JunhuiLin JianqingSong Chuangui - Pre-eclampsia (PE) involves placental dysfunction and immune dysregulation, but the cell-type localization of tryptophan-kynurenine-nicotinamide adenine dinucleotide (Trp-Kyn-NAD+) axis-related genes in PE placentas remains unclear. - Source: PubMed
Zhang YiLin XiaoxiaoYao LuCao Yingdong - Physical inactivity and mechanical unloading induce skeletal muscle atrophy and are associated with systemic metabolic disorders, but the molecular basis linking muscle disuse to liver injury remains unclear. Human cohort analyses (CHARLS, NHANES), a mouse hindlimb immobilization model, and multi-level in vitro systems were used to define this mechanism. Muscle disuse activates skeletal muscle indoleamine 2,3-dioxygenase 1 (IDO1), accompanied by altered tryptophan metabolism and increased systemic kynurenine accumulation. Kynurenine functioned as a circulating pathogenic mediator that activates hepatic aryl hydrocarbon receptor (AhR) signaling, resulting in oxidative stress, hepatocyte injury, and fibrotic remodeling. Importantly, pharmacological inhibition of IDO1 in vivo and siRNA-mediated IDO1 knockdown in vitro reduced kynurenine-associated AhR signaling and attenuated hepatocyte injury-related phenotypes. These findings identify an IDO1-kynurenine-AhR axis associated with muscle atrophy-related liver pathology and suggest that skeletal muscle IDO1 activation contributes to inter-organ metabolic communication during physical inactivity. Targeting this pathway may provide a therapeutic strategy to mitigate systemic complications associated with disuse and sedentary conditions. - Source: PubMed
Publication date: 2026/08/31
Li XiuruPeng JinglinHuang YatingYang XuegeNiu YanmeiFu Li