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γ-亚麻酸通过 PPAR-γ 信号通路改善 DHEA 诱导的多囊卵巢综合征大鼠的促炎反应。

γ-Linolenic acid ameliorates DHEA induced pro-inflammatory response in polycystic ovary syndrome via PPAR-γ signaling in rats.

机构信息

Department of Biomedical Sciences, School of Biosciences and Technology, Vellore Institute of Technology, Vellore, 632014, Tamil Nadu, India.

Department of Biomedical Sciences, School of Biosciences and Technology, Vellore Institute of Technology, Vellore, 632014, Tamil Nadu, India.

出版信息

Reprod Biol. 2020 Sep;20(3):348-356. doi: 10.1016/j.repbio.2020.05.004. Epub 2020 May 19.

DOI:10.1016/j.repbio.2020.05.004
PMID:32444273
Abstract

The inflammatory responses associated with polycystic ovary syndrome (PCOS) may play a significant role in the severity of the disease. Emerging evidence report states that the polyunsaturated fatty acids are capable of ameliorating the PCOS condition. The therapeutic effects of γ-linolenic acid (GLA), an omega-6 fatty acid, in various inflammatory diseases have been reported. Yet, its role in PCOS associated inflammatory response remains unexplored. The aim of the study was to decipher the effects of GLA in PCOS and its role in the PPAR-γ pathway. In our study, female Wistar rats were stimulated with daily subcutaneous injections of DHEA (60 mg/kg per day) for 28 days to induce PCOS. Daily doses of GLA(10, 20, and 50 mg/kg) and Pioglitazone (P)(30 mg/kg) were administered orally for 14 days after PCOS induction. The levels of DHEA, leptin, PPAR-γ were measured by ELISA. The gene expression levels of leptin, TNF-α, IL-33, PPAR-γ, C/EBP-β, SREBP-1were determined by Real Time-PCR. We observed that the GLA significantly attenuated the DHEA and leptin levels. GLA treatment also upregulated PPAR-γ expression, when compared to the DHEA group. Further, GLA treatment showed a significant reduction in DHEA induced TNF-α, IL-33, C/EBP-β, and SREBP-1 levels in Wistar rat polycystic ovary tissue samples. The present findings could indicate that GLA is able to reduce the inflammatory response due to DHEA stimulation and thereafter potentially attenuate PCOS via the PPAR-γ pathway.

摘要

多囊卵巢综合征(PCOS)相关的炎症反应可能在疾病的严重程度中起重要作用。新出现的证据表明,多不饱和脂肪酸能够改善 PCOS 状况。已经有报道称,ω-6 脂肪酸γ-亚麻酸(GLA)在各种炎症性疾病中的治疗效果。然而,其在 PCOS 相关炎症反应中的作用仍未被探索。本研究旨在阐明 GLA 在 PCOS 中的作用及其在 PPAR-γ 通路中的作用。在我们的研究中,雌性 Wistar 大鼠每天接受 DHEA(60mg/kg 每天)皮下注射 28 天以诱导 PCOS。在 PCOS 诱导后 14 天,每天口服给予 GLA(10、20 和 50mg/kg)和吡格列酮(P)(30mg/kg)。通过 ELISA 测量 DHEA、瘦素、PPAR-γ 的水平。通过实时 PCR 测定瘦素、TNF-α、IL-33、PPAR-γ、C/EBP-β、SREBP-1 的基因表达水平。我们观察到 GLA 显著减弱了 DHEA 和瘦素的水平。与 DHEA 组相比,GLA 处理还上调了 PPAR-γ 的表达。此外,GLA 治疗显示 DHEA 诱导的 TNF-α、IL-33、C/EBP-β 和 SREBP-1 在 Wistar 大鼠多囊卵巢组织样品中的水平显著降低。这些发现可能表明,GLA 能够减少 DHEA 刺激引起的炎症反应,从而通过 PPAR-γ 通路潜在地减轻 PCOS。

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