Journal of Steroid Biochemistry and Molecular Biology最新文献_第8页

Corrigendum to “Low-fat diets and testosterone in men: Systematic review and meta-analysis of intervention studies” [Journal of Steroid Biochemistry and Molecular Biology, 210 (2021) 105878] “低脂饮食和男性睾酮：干预研究的系统回顾和荟萃分析”的勘误表[Journal of steroids Biochemistry and Molecular Biology， 210(2021) 105878]。

IF 2.5 2区生物学 Q3 BIOCHEMISTRY & MOLECULAR BIOLOGY

Journal of Steroid Biochemistry and Molecular Biology

Pub Date : 2026-01-01 Epub Date: 2025-10-25 DOI: 10.1016/j.jsbmb.2025.106880

Joseph Whittaker , Kexin Wu

引用次数: 0

Bushen Huoxue formula component β-Estradiol 3-acetate treats osteoarthritis through enhancing the TLR4 ubiquitination 补肾活血方成分β-雌二醇3-醋酸酯通过增强TLR4泛素化治疗骨关节炎。

IF 2.5 2区生物学 Q3 BIOCHEMISTRY & MOLECULAR BIOLOGY

Journal of Steroid Biochemistry and Molecular Biology

Pub Date : 2026-01-01 Epub Date: 2025-09-12 DOI: 10.1016/j.jsbmb.2025.106862

Xiaoli Liu , Shan Wang , Chuangfu Kuang , Yuwen Deng , Shuaicai Yuan , Juying Zou

We aim to explore the key metabolic components and underlying mechanisms of the Bushen Huoxue Formula (BH) in treating Osteoarthritis (OA). The mouse knee OA model was constructed using the destabilization of the medial meniscus method. OA mice were orally administered the BH. Mouse cartilage damage was assessed. High performance liquid chromatography-tandem mass spectrometry (HPLC-MS), network pharmacology analysis and molecular docking were employed to analyze the serum metabolite components and target protein of BH. After lipopolysaccharide (LPS) treatment, different concentrations of β-Estradiol 3-acetate were added to primary chondrocytes. Flow cytometry was utilized for detecting cell apoptosis. The Ubiquitin-Specific Protease 13 (USP13)/Toll-like Receptor 4 (TLR4)/Myeloid Differentiation Primary Response Protein 88 (MYD88)/NF-κB pathway and the TLR4 ubiquitination levels were assessed using immunological quantification and biochemical methods. Relative to normal mice, OA mice exhibited decreased knee joint cartilage thickness and increased inflammatory damage. BH treatment reversed these effects. Furthermore, BH enhanced TLR4 ubiquitination. Estradiol acetate was identified as the metabolic component of BH that alleviates OA. Estradiol acetate and its subtype molecule β-Estradiol 3-acetate could bind to the USP13 protein. The β-Estradiol 3-acetate concentration-dependently decreased the elevated levels of USP13, TLR4, MYD88, p-p65/p65 in chondrocytes induced by LPS, while increasing the TLR4 ubiquitination. β-Estradiol 3-acetate reversed LPS-induced chondrocyte apoptosis and elevation of inflammatory factors. Moreover, USP13 overexpression abolished the protective effects of BH and β-Estradiol 3-acetate against LPS-induced chondrocytes. In Conclusion, the BH metabolite β-Estradiol 3-acetate promotes TLR4 ubiquitination to relieve inflammation and apoptosis in OA chondrocytes by inhibiting USP13.

我们旨在探讨补肾活血方治疗骨关节炎（OA）的关键代谢成分及其作用机制。采用内侧半月板失稳法建立小鼠膝关节OA模型。OA小鼠口服BH。评估小鼠软骨损伤。采用高效液相色谱-串联质谱法（HPLC-MS）、网络药理学分析、分子对接等方法对白芍血清代谢物成分和靶蛋白进行分析。脂多糖（LPS）处理后，在原代软骨细胞中加入不同浓度的β-雌二醇3-乙酸酯。流式细胞术检测细胞凋亡。采用免疫定量和生化方法评估泛素特异性蛋白酶13 (USP13)/ toll样受体4 (TLR4)/髓样分化初级反应蛋白88 (MYD88)/NF-κB通路和TLR4泛素化水平。与正常小鼠相比，OA小鼠表现出膝关节软骨厚度减少和炎症损伤增加。BH治疗逆转了这些效果。此外，BH增强了TLR4的泛素化。经鉴定，醋酸雌二醇是BH减轻OA的代谢成分。Estradiol acetate及其亚型分子β-Estradiol 3-acetate可与USP13蛋白结合。β-雌二醇3-醋酸酯浓度依赖性地降低了LPS诱导的软骨细胞中USP13、TLR4、MYD88、p-p65/p65的升高水平，同时增加了TLR4的泛素化。β-雌二醇3-醋酸酯逆转lps诱导的软骨细胞凋亡和炎症因子升高。此外，USP13过表达消除了BH和β-雌二醇3-醋酸酯对lps诱导的软骨细胞的保护作用。综上所述，BH代谢产物β-Estradiol 3-acetate通过抑制USP13，促进TLR4泛素化，减轻OA软骨细胞炎症和凋亡。

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引用次数: 0

17β-estradiol (E2) increases ciliary beat frequency via membrane estrogen receptor β 17β-雌二醇（E2）通过膜雌激素受体β增加纤毛搏动频率。

IF 2.5 2区生物学 Q3 BIOCHEMISTRY & MOLECULAR BIOLOGY

Journal of Steroid Biochemistry and Molecular Biology

Pub Date : 2026-01-01 Epub Date: 2025-09-29 DOI: 10.1016/j.jsbmb.2025.106871

Kouta Noriyama , Nobuhisa Todo , Nobuyo Tamiya , Masaki Shigeta , Yuki Toda , Shigekuni Hosogi , Eishi Ashihara

Estrogen receptors (ER) are expressed in various tissues, including the lungs and other respiratory tissues, independent of sex. However, the role of estrogen in the respiratory tract is not fully understood. Airway ciliated cells are important for mucociliary clearance (MCC), which protects the human airways from foreign substances, and ciliary beat frequency (CBF) is an important indicator of MCC efficiency. Although the function of estrogen in airway smooth muscle cells and goblet cells has been studied, its effects on airway ciliated cells remain unclear. Here, we investigated the effect of 17β-estradiol (E2) on CBF. E2 increased CBF and intracellular cAMP concentration ([cAMP]_i) in murine airway ciliated cells, whereas it had no effect on intracellular Ca^2 + concentration and intracellular pH. The selective ERβ inhibitor PHTPP suppressed the E2-induced increase in CBF and [cAMP]_i. β-Estradiol 6-(O-carboxymethyl)oxime: bovine serum albumin conjugate, which activates membrane ER, also increased CBF and [cAMP]_i in murine airway ciliated cells, and PHTPP suppressed these effects. The results of this study indicate that E2 increases CBF by increasing [cAMP]_i via membrane ERβ in murine airway ciliated cells. These results provide new insight into the function of estrogen in airway ciliated cells.

雌激素受体（ER）在各种组织中表达，包括肺和其他呼吸组织，与性别无关。然而，雌激素在呼吸道中的作用尚不完全清楚。气道纤毛细胞在粘膜纤毛清除（mucociliary clearance， MCC）中起着重要的作用，而纤毛搏动频率（ciliary beat frequency， CBF）是MCC效率的重要指标。虽然雌激素在气道平滑肌细胞和杯状细胞中的作用已被研究，但其对气道纤毛细胞的影响尚不清楚。在这里，我们研究了17β-雌二醇（E2）对CBF的影响。E2增加小鼠气道纤毛细胞的CBF和细胞内cAMP浓度（[cAMP]i），而对细胞内Ca2+浓度和细胞内ph没有影响。选择性ERβ抑制剂PHTPP抑制E2诱导的CBF和[cAMP]i的增加。β-雌二醇6-（o -羧甲基）肟：牛血清白蛋白偶联物，激活膜内质网，也增加小鼠气道纤毛细胞的CBF和[cAMP]i，而PHTPP抑制了这些作用。本研究结果表明，E2通过小鼠气道纤毛细胞膜ERβ增加[cAMP]i，从而增加CBF。这些结果为雌激素在气道纤毛细胞中的作用提供了新的认识。

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引用次数: 0

White kidney bean extract improves letrozole-induced polycystic ovary syndrome in rats by regulating the Wnt signaling pathway 白芸豆提取物通过调节Wnt信号通路改善来曲唑诱导的大鼠多囊卵巢综合征

IF 2.5 2区生物学 Q3 BIOCHEMISTRY & MOLECULAR BIOLOGY

Journal of Steroid Biochemistry and Molecular Biology

Pub Date : 2026-01-01 Epub Date: 2025-09-07 DOI: 10.1016/j.jsbmb.2025.106858

Jiani Zhu , Ran Gu , Ya Zhu , Qun Zhou , Zijuan Zhang , Xinyue Qi , Xiaorong Wu , Bo Deng , Lanping Zhong

Polycystic ovary syndrome (PCOS) is an endocrine-metabolic disorder characterized by ovarian dysfunction, with limited effective treatments. This study investigates the therapeutic effects and mechanisms of white kidney bean extract (WKBE) in a PCOS rat model. A PCOS model was established using letrozole, followed by intervention with varying doses of WKBE. Serum sex hormone levels, insulin resistance, and metabolic markers were measured. Ovarian histopathology, fibrosis, and apoptosis were assessed. Transcriptomic sequencing was performed on ovarian tissues from control, PCOS, and high-dose WKBE groups. High-dose WKBE significantly ameliorated endocrine-metabolic disturbances in PCOS rats, including reduced testosterone, LH/FSH ratio, insulin resistance, and lipid abnormalities, outperforming low/medium doses. It decreased body weight, ovarian index, and organ fat deposition, repaired ovarian histopathological damage, and reduced fibrosis and apoptosis. Transcriptomic analysis revealed that high-dose WKBE altered the expression of Wnt signaling pathway-related genes, suggesting its therapeutic role may involve modulation of this pathway. High-dose WKBE alleviates endocrine-metabolic dysregulation and ovarian dysfunction in PCOS rats by regulating the Wnt signaling pathway, offering a potential novel therapeutic strategy.

多囊卵巢综合征（PCOS）是一种以卵巢功能障碍为特征的内分泌代谢疾病，有效治疗方法有限。本研究探讨白芸豆提取物（WKBE）对PCOS大鼠模型的治疗作用及其机制。用来曲唑建立多囊卵巢综合征模型，然后用不同剂量的WKBE进行干预。测定血清性激素水平、胰岛素抵抗和代谢指标。评估卵巢组织病理学、纤维化和细胞凋亡。对对照组、PCOS组和高剂量WKBE组的卵巢组织进行转录组测序。高剂量WKBE显著改善PCOS大鼠的内分泌代谢紊乱，包括降低睾酮，LH/FSH比率，胰岛素抵抗和脂质异常，优于低/中剂量。降低体重、卵巢指数和器官脂肪沉积，修复卵巢组织病理损伤，减少纤维化和细胞凋亡。转录组学分析显示，高剂量WKBE改变了Wnt信号通路相关基因的表达，提示其治疗作用可能与调节该通路有关。大剂量WKBE通过调节Wnt信号通路减轻PCOS大鼠内分泌代谢失调和卵巢功能障碍，为PCOS大鼠提供了一种潜在的新型治疗策略。

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引用次数: 0

Excess aldosterone and cortisol promote myocardial iron deficiency: A potential pathway to cardiac injury 过量的醛固酮和皮质醇促进心肌铁缺乏：心脏损伤的潜在途径

IF 2.5 2区生物学 Q3 BIOCHEMISTRY & MOLECULAR BIOLOGY

Journal of Steroid Biochemistry and Molecular Biology

Pub Date : 2026-01-01 Epub Date: 2025-10-25 DOI: 10.1016/j.jsbmb.2025.106882

Aleksandar Cirovic

Mineralocorticoid receptor antagonists (MRAs) such as finerenone have shown clinical benefits in heart failure, yet their full mechanisms remain unclear. Recent evidence suggests a novel role of aldosterone in disrupting myocardial iron homeostasis. Aldosterone, via mineralocorticoid receptor (MR) activation, downregulates key iron transporters like transferrin receptor 1 (TfR1) through SGK1 signaling, contributing to myocardial iron deficiency (MID). Cortisol, which circulates at much higher levels than aldosterone and shares similar MR affinity, may similarly promote MID—especially in tissues like the heart where 11β-HSD2 activity is low. Iron deficiency in cardiomyocytes impairs mitochondrial function, reduces ATP synthesis, and promotes fibrosis and inflammation. MRAs may counteract these effects by restoring iron uptake and improving myocardial energetics. This emerging aldosterone–iron axis offers novel insight into the cardiac effects of MR activation and identifies iron homeostasis as a potential therapeutic target. Further research is warranted to explore MRA-mediated modulation of myocardial iron metabolism.

矿皮质激素受体拮抗剂（MRAs）如细烯酮已显示出心力衰竭的临床益处，但其完整机制尚不清楚。最近的证据表明，醛固酮在破坏心肌铁稳态中的新作用。醛固酮通过矿化皮质激素受体（MR）激活，通过SGK1信号下调转铁蛋白受体1 （TfR1）等关键铁转运蛋白，导致心肌铁缺乏（MID）。皮质醇的循环水平比醛固酮高得多，并具有相似的MR亲和力，可能同样促进mid - - -特别是在心脏等11β-HSD2活性较低的组织中。心肌细胞缺铁会损害线粒体功能，减少ATP合成，促进纤维化和炎症。mra可以通过恢复铁摄取和改善心肌能量来抵消这些影响。这一新兴的醛固酮-铁轴为MR激活对心脏的影响提供了新的见解，并将铁稳态确定为潜在的治疗靶点。mri介导的心肌铁代谢调节有待进一步研究。

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引用次数: 0

POMC mediates orofacial hyperalgesia under hypoestrogenic conditions POMC介导低雌激素条件下的口面部痛觉过敏。

IF 2.5 2区生物学 Q3 BIOCHEMISTRY & MOLECULAR BIOLOGY

Journal of Steroid Biochemistry and Molecular Biology

Pub Date : 2026-01-01 Epub Date: 2025-09-12 DOI: 10.1016/j.jsbmb.2025.106861

Cong Chen , Linqian Zhang , Wenjuan Wang , Yanrong Sun , Yu Bai , Qinhan Yao , Shuo Qin , Lihua Qin , Jing Jia

Estrogen modulates sensory neuron excitability via metabolic pathways, regulating women's pain perception. pro-opiomelanocortin (POMC), an endogenous polypeptide precursor, regulates pain response and is highly expressed in the trigeminal ganglion (TG). In this study, we used ovariectomized female rats to study how trigeminal ganglion POMC links to orofacial allodynia in hypoestrogenic state, and verified at both the gene and protein levels that the expression of POMC in the trigeminal ganglion decreased under the hypoestrogenic state. Subsequently, overexpressing the POMC gene in the TG reversed the pain hyperalgesia in ovariectomized rats. To further explore the regulatory mechanism of estrogen on POMC, we injected a selective estrogen receptor agonist at the trigeminal ganglion. Estradiol (E2) in the TG regulates the expression of POMC through estrogen receptor α (ERα). Subsequently, the Chromatin Cleavage and Tagging technology (CUT&Tag) and the dual-luciferase assay revealed that estrogen receptor α in the trigeminal ganglion has a positive regulatory effect on the promoter of POMC. In conclusion, this study has found that in the trigeminal ganglion, estrogen receptor α may reduce the expression of the POMC gene by inhibiting the activity of the POMC promoter. Meanwhile, this study has also found that in the TG, ERα may further regulate the biological activity of the POMC protein by binding to it. This dual regulation at both the transcriptional level and the protein level collectively mediates a decrease in the orofacial mechanical pain threshold and triggers an orofacial allodynia response.

雌激素通过代谢途径调节感觉神经元的兴奋性，调节女性的疼痛感知。opiomelanocortin （POMC）是一种内源性多肽前体，调节疼痛反应，并在三叉神经节（TG）中高度表达。在本研究中，我们利用去卵巢的雌性大鼠研究了低雌激素状态下三叉神经节POMC与口面异痛症的联系，并在基因和蛋白水平上证实了低雌激素状态下三叉神经节POMC的表达减少。随后，在TG中过表达POMC基因逆转了去卵巢大鼠的痛觉过敏。为了进一步探讨雌激素对POMC的调控机制，我们在三叉神经节处注射选择性雌激素受体激动剂。甘油三酯中的雌二醇（E2）通过雌激素受体α (ERα)调节POMC的表达。随后，染色质切割和标记技术（CUT&Tag）和双荧光素酶实验发现三叉神经节雌激素受体α对POMC启动子具有正调控作用。综上所述，本研究发现，在三叉神经节中，雌激素受体α可能通过抑制POMC启动子的活性来降低POMC基因的表达。同时，本研究还发现，在TG中，ERα可能通过与POMC蛋白结合，进一步调节POMC蛋白的生物活性。这种转录水平和蛋白质水平的双重调控共同介导了口面机械痛阈的降低，并引发了口面异常性痛反应。

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引用次数: 0

Inhibition of 14–3-3 protein enhances steroid hormone production and oxidative stress in mouse ovary: Implications for apoptosis regulation 14-3-3蛋白抑制小鼠卵巢类固醇激素产生和氧化应激：凋亡调控的意义。

IF 2.5 2区生物学 Q3 BIOCHEMISTRY & MOLECULAR BIOLOGY

Journal of Steroid Biochemistry and Molecular Biology

Pub Date : 2026-01-01 Epub Date: 2025-09-28 DOI: 10.1016/j.jsbmb.2025.106869

Shatrudhan Upadhyay , Namrata Dubey , Aanya Singh

The ovary is a primary reproductive organ where the fine balance between steroidogenesis, oxidative stress, and apoptosis governs female reproductive health. A highly conserved protein, 14–3–3, is known to influence steroid biosynthesis, redox balance, and cell survival; however, its integrative role in ovarian physiology remains poorly defined. This study investigated the consequences of pharmacological inhibition of 14–3–3 protein using BV02 in in vitro cultured mouse ovaries. Immunohistochemical analysis revealed strong expression of 14–3–3 in granulosa cells, with moderate expression in oocytes and theca cells. In the BV02-treated ovary (100 μM), there was significant elevation in the levels of ovarian progesterone, testosterone, and estradiol, indicating enhanced steroidogenesis. However, the treated ovaries showed decreased activity of catalase and superoxide dismutase (SOD), along with increased lipid peroxidation (TBARS), indicating increased oxidative stress. Western blot analysis showed downregulation of the anti-apoptotic protein Bcl-2 together with elevated levels of the pro-apoptotic protein Caspase-3, signifying a molecular shift toward apoptosis. Correlation analysis further established strong associations (p < 0.05) between oxidative stress markers and apoptotic regulators, highlighting a mechanistic link between impaired antioxidant defenses and apoptosis. These findings reveal that 14–3–3 protein acts as a dual regulator of ovarian physiology by restraining steroid hormone production in addition to maintaining redox balance and cell survival. Disruption of this equilibrium may lead to pathological states such as polycystic ovary syndrome (PCOS) and ovarian cancer. Thus, this study provides novel mechanistic insights into the regulatory role of 14–3–3 protein in the ovary and underscores its potential as a therapeutic target in reproductive disorders.

卵巢是主要生殖器官，甾体生成、氧化应激和细胞凋亡之间的良好平衡支配着女性生殖健康。已知高度保守的14-3-3蛋白影响类固醇生物合成、氧化还原平衡和细胞存活；然而，其在卵巢生理中的综合作用仍不明确。本研究探讨了BV02对体外培养小鼠卵巢14-3-3蛋白的药理抑制作用。免疫组化分析显示14-3-3在颗粒细胞中强表达，在卵母细胞和卵泡细胞中有中等表达。在bv02处理的卵巢（100μM）中，卵巢黄体酮、睾酮和雌二醇水平显著升高，表明类固醇生成增强。然而，处理后的卵巢过氧化氢酶和超氧化物歧化酶（SOD）活性下降，脂质过氧化（TBARS）升高，表明氧化应激增加。Western blot分析显示，抗凋亡蛋白Bcl-2下调，促凋亡蛋白Caspase-3水平升高，表明细胞向凋亡的分子转移。相关分析进一步确立了强关联(p

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引用次数: 0

7-ketocholesterol as a critical oxysterol: Impact on human health and safety in food systems 7-酮胆固醇作为一种重要的氧化固醇：对食品系统中人类健康和安全的影响。

IF 2.5 2区生物学 Q3 BIOCHEMISTRY & MOLECULAR BIOLOGY

Journal of Steroid Biochemistry and Molecular Biology

Pub Date : 2026-01-01 Epub Date: 2025-09-05 DOI: 10.1016/j.jsbmb.2025.106856

Sheethal S Kumar, Akash Prakash, P.V. Keerthana, Mathew John

7-Ketocholesterol (7-KC) is a biologically active oxysterol formed through the oxidation of cholesterol, predominantly under conditions of oxidative stress. It is generated both enzymatically in specific tissues such as the brain and liver, and non-enzymatically via reactive oxygen species (ROS), especially in aging tissues and heat-processed animal-derived foods. 7-KC exerts multifaceted effects on human health, extending beyond lipid metabolism to disrupt glucose and amino acid utilization, impair mitochondrial function, and provoke endoplasmic reticulum (ER) stress. These disturbances contribute to chronic inflammation and oxidative damage, playing pivotal roles in the development of various diseases, including atherosclerosis, neurodegenerative disorders, diabetes, cancer, hepatic steatosis, and ocular and gastrointestinal pathologies. Additionally, 7-KC is a marker of cholesterol oxidation in the food industry, where it signals product degradation and potential toxicity in long-stored or thermally processed animal-based foods. This review explores the biosynthesis, metabolic fate, and pathophysiological role of 7-KC, highlighting its critical role in intermediary metabolism, disease progression, and food safety. Furthermore, it outlines mitigation strategies to reduce 7-KC exposure through dietary modifications, antioxidant interventions, and advanced food processing technologies aimed at enhancing public health.

7-酮胆固醇（7-KC）是一种具有生物活性的氧甾醇，主要是在氧化应激条件下通过胆固醇氧化形成的。它可以在特定组织（如大脑和肝脏）中酶促产生，也可以通过活性氧（ROS）非酶促产生，特别是在老化组织和热加工的动物源性食品中。7-KC对人体健康具有多方面的影响，不仅限于脂质代谢，还可破坏葡萄糖和氨基酸的利用，损害线粒体功能，并引起内质网（ER）应激。这些紊乱导致慢性炎症和氧化损伤，在各种疾病的发展中起关键作用，包括动脉粥样硬化、神经退行性疾病、糖尿病、癌症、肝脂肪变性、眼部和胃肠道病变。此外，在食品工业中，7-KC是胆固醇氧化的标志，在长期储存或热加工的动物性食品中，它标志着产品降解和潜在毒性。本文综述了7-KC的生物合成、代谢命运和病理生理作用，重点介绍了7-KC在中间代谢、疾病进展和食品安全中的重要作用。此外，它还概述了通过饮食调整、抗氧化干预和旨在加强公众健康的先进食品加工技术来减少7-KC暴露的缓解战略。

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引用次数: 0

Advancements in understanding the role and mechanisms of mitochondria in diabetes: A comprehensive review 线粒体在糖尿病中的作用和机制研究进展综述

IF 2.5 2区生物学 Q3 BIOCHEMISTRY & MOLECULAR BIOLOGY

Journal of Steroid Biochemistry and Molecular Biology

Pub Date : 2026-01-01 Epub Date: 2025-10-06 DOI: 10.1016/j.jsbmb.2025.106875

Xia Ge , Min Ye , Aihua Fei , Qingping Zhang , Aihong Yuan

Diabetes mellitus is a global health crisis with a rising prevalence attributed to complex interactions of genetic, lifestyle, and environmental factors. This comprehensive review delves into the pivotal role of mitochondrial dysfunction in the onset and progression of diabetes. It outlines how defects in mitochondrial oxidative phosphorylation, increased free radical production, and mitochondrial DNA damage contribute to insulin resistance, β-cell apoptosis, and systemic metabolic dysfunctions. The review highlights the critical roles of mitochondria in energy metabolism, oxidative balance, and the interplay of genetic and environmental factors in diabetes. It also emphasizes the association of impaired mitochondrial function with various diabetes-related complications and organ-specific diseases, underscoring the urgent need for innovative therapeutic strategies. Potential interventions discussed include pharmacological agents promoting mitochondrial biogenesis and enhancing mitochondrial dynamics, alongside dietary and lifestyle modifications that support mitochondrial function and overall metabolic health. The review calls for intensified research into mitochondrial mechanisms and their therapeutic targets, advocating for comprehensive clinical trials and support from medical and governmental institutions to advance diabetes management strategies centered on mitochondrial health.

糖尿病是一种全球性的健康危机，由于遗传、生活方式和环境因素的复杂相互作用，其患病率不断上升。这篇综合综述深入研究了线粒体功能障碍在糖尿病发病和进展中的关键作用。它概述了线粒体氧化磷酸化缺陷、自由基产生增加和线粒体DNA损伤如何导致胰岛素抵抗、β细胞凋亡和全身代谢功能障碍。这篇综述强调了线粒体在糖尿病的能量代谢、氧化平衡以及遗传和环境因素的相互作用中的关键作用。它还强调了线粒体功能受损与各种糖尿病相关并发症和器官特异性疾病的关联，强调了迫切需要创新的治疗策略。讨论的潜在干预措施包括促进线粒体生物发生和增强线粒体动力学的药理学药物，以及支持线粒体功能和整体代谢健康的饮食和生活方式改变。该综述呼吁加强对线粒体机制及其治疗靶点的研究，倡导全面的临床试验和医疗和政府机构的支持，以推进以线粒体健康为中心的糖尿病管理策略。

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引用次数: 0

Zingerone supplementation affects proliferation, apoptosis, antioxidant, GLUT4 and insulin receptor expression in uterus of mice 补充姜酮对小鼠子宫增殖、凋亡、抗氧化及GLUT4和胰岛素受体表达有影响。

IF 2.5 2区生物学 Q3 BIOCHEMISTRY & MOLECULAR BIOLOGY

Journal of Steroid Biochemistry and Molecular Biology

Pub Date : 2026-01-01 Epub Date: 2025-10-30 DOI: 10.1016/j.jsbmb.2025.106885

Ayushmita Dutta, Guruswami Gurusubramanian, Vikas Kumar Roy

Zingerone has various biological properties with a modulatory role in ovarian activity. Despite its biological property, its effect has not been investigated on the uterus. Therefore, the present study has investigated the effects of zingerone supplementation on uterus of mice. Female Swiss albino mice were randomly divided into four groups: control, Z10, Z25, and Z50, where zingerone was orally given for 28 days. Zingerone treatment at 25 and 50 mg/kg increased the number of uterine glands. Immunolocalization of PCNA was decreased in the in vivo study, while in vitro BrdU incorporation was stimulated by the zingerone. Zingerone treatment increased apoptosis at a 25 mg/kg dose; however, zingerone at a 50 mg/kg dose decreased uterine apoptosis. In vitro study also showed zingerone down-regulates BCL2 expression and up-regulates active caspase expression. These findings suggest modulatory effects of zingerone on uterine proliferation and apoptosis. The pro-inflammatory TNFα showed the lowest expression in 50 mg/kg zingerone-treated mice uterus. In vitro findings also showed that zingerone decreased expression of TNFα. Furthermore, an in vivo study has also shown zingerone down-regulates INSR and GLUT4 without affecting uterine glucose concentration. In addition, an in vitro study has also shown that zingerone down-regulates INSR. Zingerone treatment showed elevated MDA levels and GPX enzyme activity. However, SOD activity was suppressed in 25 and 50 mg/kg groups. Furthermore, catalase activity was highest in the 50 mg/kg zingerone-treated group. Thus, these results showed the modulatory role of zingerone on apoptosis, glucose metabolism, and antioxidant status in uterus. The functional significance of zingerone-mediated parameters on uterine functions remains to be investigated.

生姜酮具有多种生物学特性，对卵巢活性具有调节作用。尽管其具有生物学特性，但其对子宫的影响尚未被研究。因此，本研究探讨了补充生姜酮对小鼠子宫的影响。雌性瑞士白化病小鼠随机分为对照组、Z10组、Z25组和Z50组，每组口服青姜酮28 d。生姜酮25、50mg/kg组大鼠子宫腺数量增加。在体内研究中，PCNA的免疫定位降低，而在体外，生姜酮刺激BrdU掺入。25mg/kg剂量的姜酮增加了细胞凋亡；50mg/kg剂量的姜酮可抑制子宫细胞凋亡。体外研究也显示姜酮下调BCL2表达，上调活性caspase表达。提示姜酮对子宫增殖和细胞凋亡具有调节作用。促炎TNFα在50mg/kg黄酮处理小鼠子宫中表达最低。体外实验结果也显示姜酮能降低TNFα的表达。此外，一项体内研究也表明生姜酮下调INSR和GLUT4而不影响子宫葡萄糖浓度。此外，一项体外研究也表明，生姜酮下调INSR。生姜酮处理后，MDA水平和GPX酶活性均升高。25和50mg/kg组SOD活性受到抑制。过氧化氢酶活性以50mg/kg姜酮处理组最高。由此可见，姜酮对子宫细胞凋亡、糖代谢和抗氧化的调节作用。黄酮介导的参数对子宫功能的功能意义有待进一步研究。

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引用次数: 0