Ask about this productRelated genes to: HSD11B1 antibody
- Gene:
- HSD11B1 NIH gene
- Name:
- hydroxysteroid 11-beta dehydrogenase 1
- Previous symbol:
- HSD11B, HSD11
- Synonyms:
- SDR26C1
- Chromosome:
- 1q32.2
- Locus Type:
- gene with protein product
- Date approved:
- 1991-11-14
- Date modifiied:
- 2016-10-05
Related products to: HSD11B1 antibody
Related articles to: HSD11B1 antibody
- Psoriasis is an immune-mediated chronic inflammatory skin disease. Radix Rehmanniae Praeparata (RRP) is a traditional Chinese medicine with abundant biological functions. This study was performed to analyze the potential functional mechanism of RRP using network pharmacology, machine learning, molecular docking, and cell experiments. Active ingredients of RRP were screened from the TCMSP database, and targets were obtained from TCMSP and Swiss Target Prediction. Targets of psoriasis were acquired from GSE274560, GeneCards, and CTD. The protein-protein interaction network was analyzed by the String website. KEGG, Reactome, and GO were analyzed to predict possible pathways. LASSO and SVM-RFE machine learning algorithms were used to screen significant targets. Interaction between active ingredients and core targets was validated by molecular docking and molecular dynamics simulation. In vitro cell experiments were conducted using human keratinocytes HaCaT, including CCK-8, Western blotting, EdU, and ELISA. Sitosterol and Stigmasterol acted as the active ingredients of RRP. A total of 145 targets for the two ingredients were screened, and 18,871 targets were obtained for psoriasis. Furthermore, 27 intersection targets were considered as the candidate target genes of RRP for psoriasis treatment. LASSO and SVM-RFE identified RORC and HSD11B1 as core targets. Molecular docking showed the binding between Sitosterol or Stigmasterol and RORC or HSD11B1. Molecular dynamics simulation further validated the binding between Stigmasterol and RORC or HSD11B1. Cell experiments indicated that Stigmasterol inhibited HaCaT proliferation and inflammation via inducing HSD11B1 upregulation. These findings demonstrate that the mechanism of RRP in psoriasis is multi-target and multi-pathway. This study has unraveled the preliminary mechanism of RRP in treating psoriasis, which involves Stigmasterol-mediated HSD11B1 upregulation. - Source: PubMed
Zhang TingtingWei LipingLiu HaoenZhou Bin - Post-weaning diarrhea remains a major challenge without noninvasive diagnostic tools. Fecal biomarkers represent a promising alternative, as they reflect gut inflammation without invasive sampling. This study evaluated four biomarkers-calprotectin (fCal), lipocalin-2 (LCN-2), myeloperoxidase (MPO), and adenosine deaminase (ADA)-using a zinc oxide (ZnO) model to assess their value as gut-health indicators in piglets. A total of 384 weaned piglets (23 d) were assigned to two diets: Control and ZnO-supplemented (1 g/kg feed). Piglets were weighed on d 0, 3, 8, and 14. On d 3 and 14, nine average-weight piglets per group were sampled for feces and intestinal tissue. Calprotectin was measured by immunoturbidimetry, MPO byss o-dianisidine oxidation, ADA by enzymatic colorimetry, and LCN-2 by ELISA. Microbiota was analyzed by 16S sequencing and tissues by qPCR and histology. On d 3, ZnO piglets showed fewer intraepithelial lymphocytes (P = 0.062), higher IL-10 expression (P = 0.029), and lower Escherichia-Shigella abundance (P = 0.045). By d 14, they were ∼300 g heavier (P = 0.071), had higher villus-to-crypt ratios (P = 0.026), maintained IL-10 upregulation (P = 0.083), and increased OCLN expression (P < 0.001). Their microbiota shifted toward Odoribacter and Akkermansia (P ≤ 0.002), with reductions in Clostridium sensu stricto 1 (P < 0.001). fCal and LCN-2 were reduced in the ZnO group on d 3 (P ≤ 0.002), but only fCal remained reduced by d 14 (P = 0.012). No diet effects were observed for MPO or ADA (P > 0.05). On d 3, fCal correlated with CRHR1 (R = 0.59, P = 0.025) and negatively with barrier-related genes MUC13 and OCLN (R ≤ -0.50, P ≤ 0.050). MPO tended to correlate with CRHR1, crypt depth (R ≥ 0.44, P ≤ 0.069), and Streptococcus abundance (R = 0.45, P = 0.073). LCN-2 was negatively associated with inflammatory genes, such as TNF-α and NF-κB (R ≤ -0.55, P ≤ 0.041). ADA showed positive trends with potentially pathogenic phyla, such as Campilobacterota (R ≥ 0.43, P ≤ 0.084). By d 14, fCal, LCN-2, and MPO were correlated with immune-related genes (eg TNF-α, TGF-β; R ≥ 0.52, P ≤ 0.071), while ADA was associated with the stress-related gene HSD11B1 (R = 0.74, P = 0.002). Overall, fecal biomarkers were valuable indicators of post-weaning gut inflammation and barrier function. Specifically, fCal was the most consistent, LCN-2 and MPO may serve complementary roles, whereas ADA primarily reflected cellular stress rather than inflammation. - Source: PubMed
Suppi JúliaLlauradó-Calero EudaldComa JaumePelegrí-Pineda AnnaSaco YolandaBassols AnnaSolà-Oriol David - This study aimed to elucidate the mechanism of San Jie Tong Mai Formula (SJTMF) against atherosclerosis (AS), a leading cause of cardiovascular morbidity. Using ApoE mouse models, we demonstrated that SJTMF significantly inhibits AS plaque progression. Through an integrated network pharmacology and proteomics strategy, five core bioactive components were identified: beta-sitosterol, naringenin, luteolin, isorhamnetin, and 3beta-hydroxy-24-methylene-8-lanostene-21-oic acid. Concurrently, proteomics revealed 129 AS-related proteins that were differentially expressed. Molecular docking confirmed high-affinity binding interactions between these components and the key target Hsd11b1, with their binding energies all below -5 kcal/mol. Mechanistic investigations further revealed that SJTMF may regulate Hsd11b1-mediated glucocorticoid metabolism. This regulation contributes to significant amelioration of both dyslipidemia and vascular inflammation, thereby suppressing AS development. Collectively, this work demonstrates, for the first time, the innovative mechanism by which a traditional Chinese medicine formula exerts anti-AS effects through multi-component synergistic regulation of the Hsd11b1 target, offering new insights for therapeutic intervention. - Source: PubMed
Publication date: 2026/04/17
Han HuizeLi HongyuZhou ZhilinLiu AidongZhong CongboSun Ye - Depression remains a leading cause of global disability, with early-life stress (ELS) representing one of its most potent and well-replicated risk factors. This chapter synthesizes evidence linking childhood adversity-including abuse, neglect, and loss-to persistent dysregulation of the hypothalamic-pituitary-adrenal (HPA) axis. A key mechanism is the imbalance between mineralocorticoid (MR) and glucocorticoid receptors (GR), resulting in altered cortisol rhythms, impaired stress recovery, and increased susceptibility to recurrent and treatment-resistant depression. Converging neuroimaging, molecular, and epigenetic data reveals that ELS induces lasting changes in MR/GR signaling, including methylation and HSD11B1 polymorphisms, which biologically embed risk across the lifespan. Translational tools such as the prednisolone suppression test (PST) and cortisol awakening response (CAR) have emerged as promising biomarkers for patient stratification, treatment prediction, and suicide risk assessment. Future directions highlight the potential of biomarker-guided psychiatry, integrating endocrine, genetic, epigenetic, neuroimaging, and immune data to inform mechanism-based interventions-such as MR/GR agonists and antagonists, including an epigenetic approach-aimed at mitigating the enduring impact of childhood adversity and advancing precision mental health care. - Source: PubMed
Juruena Mario F - Bone and skeletal muscles are vital to human health, and diseases related to these tissues can place significant stress on patients, families, and society. The key enzyme regulating glucocorticoid metabolism, 11β-hydroxysteroid dehydrogenase 1 (11β-HSD1), is encoded by the gene and can convert inactive cortisone into active cortisol. Recent studies have shown that 11β-HSD1 is a key enzyme in the pathogenesis of bone and skeletal muscle, with its function being strictly context-dependent. 11β-HSD1 inhibits osteoblast differentiation and activates osteoclast formation, contributing to glucocorticoid-induced osteoporosis (GIOP). 11β-HSD1 accelerates skeletal muscle atrophy by disrupting the stability of muscle proteins. It plays a dual role in anti-inflammation and bone protection, participating in polyarthritis; 11β-HSD1 also contributes to bone loss and anti-inflammation in rheumatoid arthritis (RA) through multiple pathways. Clarifying the context-specific mechanisms of 11β-HSD1 in bone and skeletal muscle diseases is critical for clinical translation. This review systematically summarizes the role of 11β-HSD1 in bone and skeletal muscle diseases, outlines its potential as a disease-specific therapeutic target, and provides new insights for precise treatment of these diseases. - Source: PubMed
Publication date: 2026/03/15
Huo LiyueSui WeiWang ShangZhu WeiYang YanweiZhang XiaolinZhang YubeiWang Xuefeng