INDO_1,AM ESTER,100UG
- Known as:
- INDO_1,AM ESTER,100UG
- Catalog number:
- 50043
- Product Quantity:
- 10 ST
- Category:
- -
- Supplier:
- Biotium
- Gene target:
- INDO_1 ESTER 100UG
Related products to: INDO_1,AM ESTER,100UG
Related articles to: INDO_1,AM ESTER,100UG
- Metabolic associated fatty liver disease (MAFLD) has high morbidity and tragically lacks effective therapeutic remedies. Tormentic acid (TA) has been shown to have therapeutic effect on liver fibrosis, but its role in MAFLD remains unknown. Therefore, we employed multi-omics analyses to investigate the effects of TA on MAFLD. In this study, male C57BL/6J mice were fed a methionine- and choline- deficiency (MCD) diet to induce MAFLD and subsequently treated with TA for 4 weeks. The therapeutic efficacy of TA was then evaluated through histopathological examination and biochemical analysis. In addition, multi-omics analyses including transcriptomics, proteomics and metabolomics were conducted to identify potential pathways associated with TA treatment. Finally, key genes and proteins in the identified pathways were validated by qPCR and Western blot. Our results showed that TA significantly alleviated liver damage and excessive lipid accumulation. Importantly, our integrative multi-omics analyses identified tryptophan metabolism and glycolysis as pivotal pathways associated with TA treatment in our fatty liver mouse model. Subsequent validation demonstrated the TA-induced upregulation of IDO2 and HAAO, suggesting engagement of tryptophan metabolism. Concurrently, TA treatment downregulated HK2, PFKP, and PKM2, indicative of altered rate-limiting glycolytic enzyme expression. These findings suggest that TA alleviates MCD diet-induced MAFLD, potentially involving modulation of enzyme expression in tryptophan metabolism and glycolysis. - Source: PubMed
Wei YuanyuanWei DingyiLu JingyangWei LulinLin WeijiaWei JinbinMa Xiao - Sheep seasonal reproduction is regulated by photoperiod via melatonin. Indoleamine 2,3-dioxygenase 2 (IDO2), an enzyme involved in tryptophan metabolism through the kynurenine pathway and belonging to the IDO family, may contribute to melatonin homeostasis, but its role in reproductive seasonality remains unclear. In this study, genome-wide selection analyses combining Z(F) and XP-EHH between seasonal and non-seasonal sheep identified a selection signature encompassing the IDO2 region and revealed g.-809T>C as a functional candidate variant within this region. Experiments employing electrophoretic mobility shift assay (EMSA) and luciferase assays revealed that this site lies within the CLOCK transcription factor binding domain. The -809C variant reduced promoter activity compared to -809T (p < 0.05). Sheep with the CC genotype had higher plasma melatonin levels than TC/TT counterparts (p < 0.05). These findings suggest that the g.-809C allele decreases IDO2 transcription by reducing CLOCK binding affinity, thereby potentially affecting IDO2-associated tryptophan/melatonin metabolism and increasing melatonin levels, which may contribute to photoperiodic responses in sheep. This IDO2 variation provides new insights into the genetic regulation of melatonin-mediated reproductive seasonality and represents a potential marker for genetic improvement of reproductive seasonal traits in sheep. - Source: PubMed
Jiang XunpingChi ShaxuanWang XiaodongChen MengyaTie ZhuoyingYang HuiguoWang ChaoliLiu Guiqiong - Colorectal cancer (CRC) progression is driven by metastatic potential, metabolic reprogramming, and immune evasion. In this study, we investigated the effects of a di-rhamnolipid, Rha-C-C (1), on CRC cell motility, energy metabolism, and immune-related signaling. Compound 1 exhibited minimal cytotoxicity in AGS, A549, and MDA-MB-231 cells, while modestly reducing viability in Caco2 cells at higher concentrations. Notably, it significantly suppressed invasion and migration, with the most pronounced effects observed in Caco2 cells. These effects were associated with downregulation of mesenchymal markers, including N-cadherin and transcription factors Snail and Slug, as well as matrix metalloproteinases (MMP2, MMP3, and MMP9), accompanied by increased TIMP2 expression. In addition, compound 1 attenuated metabolic activity by reducing the expression of key glycolytic regulators, including GLUT1, LDHA, and HK2. It also suppressed immune evasion-related factors such as PD-L1, IDO1, IDO2, and Galectin. Mechanistic investigations using BaP and the AKT inhibitor MK2206 suggest that the effects of compound 1 involve modulation of AKT-associated signaling while also engaging additional regulatory pathways. Collectively, these findings demonstrate that compound 1 suppresses colorectal cancer cell motility, metabolic activity, and immune evasion, highlighting its potential as a natural compound targeting multiple tumor-promoting processes. - Source: PubMed
Pulat SultanHillman Prima FKo JaeyoungNam Sang-JipKim Hangun - Hyperuricemia (HUA) is increasingly recognized as a systemic inflammatory-metabolic disorder that contributes to immune-associated renal injury. Kynurenic acid (KYNA), a tryptophan-derived metabolite with reported immunomodulatory properties, has emerged as a potential mediator linking gut metabolism and distal organ inflammation. In this study, we investigated the protective effects of astilbin (ASB) against HUA and hyperuricemia-associated renal injury using an adenine-induced goose model, which is translationally relevant because geese naturally lack functional uricase, together with monosodium urate (MSU)-challenged primary renal tubular epithelial cells. By integrating multi-omics analyses, molecular docking, and molecular biology approaches, we found that ASB reduced serum uric acid, improved renal function, and attenuated inflammatory and fibrotic changes in vivo. ASB also suppressed circulating pro-inflammatory cytokines, restored intestinal barrier-related markers, and partially corrected gut microbial dysbiosis. Untargeted metabolomics revealed that KYNA was markedly reduced under HUA conditions and was restored by ASB treatment in both intestinal contents and serum. In parallel, ASB increased IDO2 expression in intestinal and hepatic tissues. In vitro, both ASB and KYNA attenuated MSU-induced inflammatory responses, restored urate transporter expression, and suppressed TGF-β/Smad-associated profibrotic signaling in primary renal cells. Collectively, these findings support a working model in which ASB ameliorates hyperuricemia-associated sterile inflammation and renal injury partly in association with gut-linked KYNA immunometabolic remodeling, accompanied by increased IDO2 expression. Because IDO1, kynurenine, KAT activity, and receptor/pathway inhibition were not assessed, the proposed mechanism should be regarded as hypothesis-supporting rather than definitively proven. - Source: PubMed
Publication date: 2026/06/19
Yang YuFei ShanshanYang LiZhang QiCui MengranShi Guangliang - Our prior research identified MO-IPS as a potent MYC-PRMT inhibitor. Here, we re-evaluated its efficacy at optimized lower doses to explore a wider therapeutic window. MO-IPS retained robust anti-proliferative activity in vitro at reduced exposures. In MV-4-11 xenografts, the higher established dose suppressed tumor growth by 72.3% and enabled metabolomic profiling. This revealed a sequential mechanism: rapid MYC suppression followed by delayed downregulation of metabolic enzymes, inducing concurrent disruption of heme biosynthesis and NAD⁺ metabolism. Molecular docking predicted potential binding to UPP1, GAMT, and IDO2, and we observed that MO-IPS downregulates their expression at mRNA and protein levels. Critically, in an immunocompetent C1498 model, a lower, therapeutically relevant dose of MO-IPS (20 mg/kg), titrated to minimize direct cytotoxicity, synergized with PD-1 therapy achieving 68.1% tumor inhibition. Mechanistically, the combination enhanced CD8⁺ T cell infiltration and reduced Treg accumulation, leading to an elevated CD8/Foxp3 ratio. This pivotal finding demonstrates that at reduced exposure, MO-IPS's anti-leukemic efficacy is driven not by overt cytotoxicity but by metabolic reprogramming that establishes a pro-immunogenic tumor microenvironment. Collectively, our work repositions MO-IPS from a cytotoxic MYC-PRMT inhibitor to a multifaceted immunometabolic therapeutic. At optimized lower doses, it orchestrates a coordinated disruption of cancer metabolic vulnerabilities and actively augments anti-tumor immunity, presenting a refined and highly promising combinatorial strategy for AML. - Source: PubMed
Publication date: 2026/06/17
Wang YingwenZhao WenjunJin YanruiHu ChenFang XingqiDong ShuhongZhang Baolai