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墨水减轻多囊卵巢综合征小鼠模型中脱氢表雄酮诱导的胰岛素抵抗。

Ink Mitigates Dehydroepiandrosterone-Induced Insulin Resistance in Mouse Model of Polycystic Ovarian Syndrome.

作者信息

Yamarthi Prathyusha, Kotipalli Rama Satyasri, Patnaik Samatasai, Veena Kv, Kathirvel Muralidharan, Vutukuri Rajkumar, Bhanoori Manjula

机构信息

Department of Biochemistry, Osmania University, Hyderabad 500007, India.

Applied Biology, CSIR-Indian Institute of Chemical Technology, Hyderabad 500007, India.

出版信息

Pathophysiology. 2024 Aug 15;31(3):408-419. doi: 10.3390/pathophysiology31030031.

DOI:10.3390/pathophysiology31030031
PMID:39189167
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11348200/
Abstract

The present study aims to evaluate the effect of ink on insulin resistance in PCOS-induced mice. Treatment with sepia ink in dehydroepiandrosterone (DHEA)-induced PCOS mice at various doses of 50 mg/kg, 100 mg/kg, and 200 mg/kg body weight mitigated the insulin resistance in the study groups with decreased concentration of testosterone and increased concentrations of estrogen and progesterone compared to the PCOS group tested by ELISA. The histopathological analysis and restoration of glucose analysis showed a significant reduction in treatment groups. Reduced expression of insulin resistance genes like androgen receptor (AR), insulin receptor substrate 1 (IRS-1), and insulin-like growth factor1 (IGF-1) by qRT-PCR indicate a positive impact of sepia ink in alleviating the symptoms associated with PCOS. Taken together, the results of this study indicate sepia ink as a promising therapeutic intervention and a possible drug target for insulin resistance in diabetes and gynecological disorders like PCOS.

摘要

本研究旨在评估乌贼墨对多囊卵巢综合征(PCOS)诱导的小鼠胰岛素抵抗的影响。通过酶联免疫吸附测定法(ELISA)检测,与PCOS组相比,用不同剂量(50毫克/千克、100毫克/千克和200毫克/千克体重)的乌贼墨处理脱氢表雄酮(DHEA)诱导的PCOS小鼠,可减轻研究组的胰岛素抵抗,同时降低睾酮浓度,提高雌激素和孕酮浓度。组织病理学分析和葡萄糖分析结果显示,治疗组有显著改善。通过实时定量聚合酶链反应(qRT-PCR)检测发现,雄激素受体(AR)、胰岛素受体底物1(IRS-1)和胰岛素样生长因子1(IGF-1)等胰岛素抵抗相关基因的表达降低,表明乌贼墨对缓解PCOS相关症状有积极作用。综上所述,本研究结果表明,乌贼墨有望成为治疗糖尿病和PCOS等妇科疾病中胰岛素抵抗的治疗干预手段和潜在药物靶点。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7b54/11348200/ae0385845557/pathophysiology-31-00031-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7b54/11348200/461ef5f5ccca/pathophysiology-31-00031-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7b54/11348200/ed42c2642511/pathophysiology-31-00031-g002a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7b54/11348200/67c71c792476/pathophysiology-31-00031-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7b54/11348200/3bc27a41ed7a/pathophysiology-31-00031-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7b54/11348200/ae0385845557/pathophysiology-31-00031-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7b54/11348200/461ef5f5ccca/pathophysiology-31-00031-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7b54/11348200/ed42c2642511/pathophysiology-31-00031-g002a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7b54/11348200/67c71c792476/pathophysiology-31-00031-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7b54/11348200/3bc27a41ed7a/pathophysiology-31-00031-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7b54/11348200/ae0385845557/pathophysiology-31-00031-g005.jpg

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引用本文的文献

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Correction: Yamarthi et al. Ink Mitigates Dehydroepiandrosterone-Induced Insulin Resistance in Mouse Model of Polycystic Ovarian Syndrome. 2024, , 408-419.更正:Yamarthi等人。《墨水减轻多囊卵巢综合征小鼠模型中脱氢表雄酮诱导的胰岛素抵抗》。2024年,第408 - 419页。
Pathophysiology. 2025 Jan 20;32(1):4. doi: 10.3390/pathophysiology32010004.

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Biochanin-A attenuates DHEA-induced polycystic ovary syndrome via upregulation of GDF9 and BMP15 signaling in vivo.生物查尔酮 A 通过上调体内 GDF9 和 BMP15 信号通路来减轻 DHEA 诱导的多囊卵巢综合征。
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