HSD17B1 is favors the reduction of estrogens and androgens. It also has 20-alpha-HSD activity. It uses preferentially NADH.
- Known as:
- HSD17B1 favors reduction estrogens androgens. 20-a-HSD activity. uses preferentially NADH.
- Catalog number:
- 29-632
- Product Quantity:
- 0.05 mg
- Category:
- -
- Supplier:
- Prosci
- Gene target:
- HSD17B1 favors the reduction estrogens and androgens. also has 20-alpha-HSD activity. uses preferentially NADH.
Related genes to: HSD17B1 is favors the reduction of estrogens and androgens. It also has 20-alpha-HSD activity. It uses preferentially NADH.
- Gene:
- HSD17B1 NIH gene
- Name:
- hydroxysteroid 17-beta dehydrogenase 1
- Previous symbol:
- EDHB17, EDH17B2
- Synonyms:
- HSD17, MGC138140, SDR28C1
- Chromosome:
- 17q21.2
- Locus Type:
- gene with protein product
- Date approved:
- 1991-06-05
- Date modifiied:
- 2016-06-03
- Gene:
- NDUFA6 NIH gene
- Name:
- NADH:ubiquinone oxidoreductase subunit A6
- Previous symbol:
- -
- Synonyms:
- B14, LYRM6, CI-B14, NADHB14
- Chromosome:
- 22q13.2
- Locus Type:
- gene with protein product
- Date approved:
- 1996-08-30
- Date modifiied:
- 2015-11-20
Related products to: HSD17B1 is favors the reduction of estrogens and androgens. It also has 20-alpha-HSD activity. It uses preferentially NADH.
Related articles to: HSD17B1 is favors the reduction of estrogens and androgens. It also has 20-alpha-HSD activity. It uses preferentially NADH.
- A better understanding of the response of granulosa cells to exogenous hormone stimulation and how this impacts the complex interplay between the granulosa cells and the oocyte is crucial for the optimal management of infertile couples seeking IVF treatment. - Source: PubMed
Publication date: 2026/06/10
Medica AlexaKim Matthew EHung Wei-TingSohni AbhishekDuleba AntoniTan KunWilkinson Miles F - Dehydroepiandrosterone (DHEA) plays a crucial role in cardiovascular physiology, while decreased plasma level of DHEA is linked to hypertension and other disorders. Curcuma longa is a globally recognized Indian medicinal plant with cardioprotective potential, but its role in DHEA restoration has not been studied yet. The present study aimed to determine whether a curcuminoid-enriched extract of Curcuma longa (CEECL) can restore serum DHEA levels and modulate DHEA biosynthetic pathways in hypertensive rodent models. L-NAME-induced Hypertension in Wistar rats and Spontaneous Hypertensive Rats (SHR) models were used to assess the effect of CEECL (100, 333, and 1000 mg/kg) using ELISA to estimate the level of circulating DHEA in serum, RT-PCR and immunohistochemistry in quantifying the expression profile of genes and of enzymes associated with DHEA biosynthesis and LC-MS for quantification of DHEA precursors and metabolites. The safety profile of CEECL was evaluated in Swiss albino mice. The study revealed a significant decline in serum DHEA levels in hypertensive conditions, and CEECL treatment restored circulating DHEA levels, improving systolic, diastolic, and mean arterial pressure in both models. Hepatic expression of key enzymes, such as CYP11A1, CYP17A1, and HSD17B1, was normalized after CEECL treatment, including the restoration of DHEA precursor levels. CEECL was well-tolerated in acute and sub-acute toxicity studies in Swiss albino mice. The current study is the first to report the restoration of DHEA biosynthesis and improvement in hemodynamics by curcuminoids-enriched C. longa extract, without the need for exogenous DHEA administration, suggesting therapeutic potential in the management of hypertension. - Source: PubMed
Publication date: 2026/06/25
Mishra DivyaIqbal HinaYadav PankajGupta ShashwatLahane VaibhaviSingh DikshaIshteyaque SharmeenMaurya Anil KumarKumar NarendraTandon SudeepGupta Anil KumarMugale Madhav NilakanthYadav Akhilesh KumarPal AnirbanShanker KarunaNegi Arvind SinghChanda Debabrata - Whether estrone (E1)-associated disruption of early reproductive development in fish is accompanied by brain responses in addition to direct gonadal effects remains unclear. Here, juvenile Siniperca chuatsi, a non-model but economically important freshwater species, were exposed for 60 d to 0, 0.01, 0.1, and 1.0 μg/L E1, spanning environmentally reported and elevated concentrations. By integrating waterborne concentration monitoring, histopathology, transcriptomics, and quantitative real-time PCR (qPCR) validation, we evaluated E1-associated changes in brain and gonadal tissues during early reproductive development. Waterborne E1 concentrations remained generally stable throughout the exposure period. At the highest tested concentration (1.0 μg/L), E1 caused neuronal vacuolation and pyknosis in the hypothalamic region and induced distinct ovarian-like structures in the gonads of genetic males. In the brain, cyp19a1, crhr1, and adcy2a were significantly upregulated, whereas egr1 was significantly downregulated, indicating transcriptional changes in genes associated with local estrogen conversion, stress-response/cAMP signaling, and neuronal activity-related regulation within a broader injury/stress-response background. In the gonad, RNA-seq analysis showed significant downregulation of star2, hsd3b1, cyp17a1, and cyp11b and significant upregulation of hsd17b1, suggesting alterations in steroidogenesis-related gene expression at the transcriptomic level. qPCR analysis of selected gonadal candidate genes showed expression directions generally consistent with the RNA-seq results, and these molecular patterns were consistent with the feminized histological phenotype. Together, these results indicate that E1 can disrupt early reproductive development in juvenile S. chuatsi and support a cautious working model in which E1 exposure is accompanied by concurrent brain and gonadal responses. This study provides new evidence for understanding the toxic effects and ecological risk implications of natural estrogen E1 during early fish development. - Source: PubMed
Publication date: 2026/06/10
Nie LeiZhang YongqingYan WeisongLi WeibinYang HaiyingDeng ZiyanCai GuojunXie ZihangLi QiangHan Chong - Alzheimer's disease (AD) is characterized not only by neuronal dysfunction but also by profound remodeling of the brain microenvironment, including immune-glial activation and metabolic dysregulation. Increasing evidence also implicates neurosteroid-related pathways in AD and dementia. Nobiletin has shown neuroprotective effects in AD-related models, but its upstream human targets and mechanism-based translational relevance remain insufficiently defined. Here, we integrated multi-omics analyses, interpretable machine learning, causal inference, structural modeling, and experimental validation to identify candidate nobiletin-associated molecular nodes in AD. HSD17B1 consistently emerged as a central AD-associated candidate across multiple analytical layers and showed reproducible discriminatory performance in independent validation cohorts. SHAP analysis further identified HSD17B1 as a major contributor to the optimal predictive model, while Mendelian randomization supported a protective association between genetically increased HSD17B1 expression and AD risk. Immune infiltration, single-cell, and spatial transcriptomic analyses linked HSD17B1 to glia-associated remodeling and regionally heterogeneous expression patterns in AD. Molecular docking and molecular dynamics simulations supported the structural feasibility of nobiletin binding to HSD17B1, and in an Aβ1-42-induced SH-SY5Y cell model, nobiletin increased HSD17B1 expression at both the mRNA and protein levels. Together, these findings support HSD17B1 as an AD-associated and nobiletin-responsive candidate molecular node, highlight a potential connection between nobiletin and neurosteroid-related regulation, and provide an integrated framework for target prioritization and validation in AD. - Source: PubMed
Publication date: 2026/05/25
Gao RenjieLyu ChenquGu YumengHao RuixiaoWang ChaoLi Xin - 17β-Hydroxysteroid dehydrogenase type 1 (HSD17B1) is a crucial enzyme in the family of 17β-hydroxysteroid dehydrogenases, serving as one of the primary activators of estrogens. Its physiological significance is highlighted by its involvement in a wide range of estrogen-related conditions, including benign diseases and hormone-dependent cancers. Consequently, the development of selective inhibitors for HSD17B1 has attracted sustained interest for several decades. Numerous lead compounds have been identified, and various strategies for reversible inhibition have been explored, reflecting the complexity of modulating estrogen biosynthesis without causing unwanted side effects. This review focuses on advances made since 2018, highlighting how research has continued to refine existing leads by improving potency, enhancing metabolic stability, and minimising estrogenic activity. In addition to optimising known scaffolds, novel directions have emerged, such as designing compounds capable of dual targeting across different enzymes involved in estrogen formation and introducing new structural scaffolds. The inhibitor candidates identified in recent years can be grouped into five distinct subcategories, each representing a different approach to reversible HSD17B1 inhibition. To provide a comparative perspective, representative compounds from these categories have been evaluated using molecular dynamics simulations, offering insight into binding behaviour and mechanistic differences. - Source: PubMed
Publication date: 2026/05/26
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