Costunolide, an effective agent against oxidative damage, apoptosis and autophagy in the ovarian torsion/detorsion model.

IF 2.5 4区 医学 Q3 ENDOCRINOLOGY & METABOLISM
Pakistan Armin Akış, Ayhan Tanyeli, Fazile Nur Ekinci Akdemir, Mustafa Can Güler, Saime Özbek Şebin, Ersen Eraslan, Esra Laloğlu, Selim Çomaklı
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引用次数: 0

Abstract

Aim: This study assessed the efficacy of costunolide (COST) against oxidative tissue damage in the ovarian torsion/detorsion (TD) model.

Methodology: Animals were randomly assigned to sham, ovarian TD, COST 5 mg/kg + ovarian TD, and COST 10 mg/kg + ovarian TD groups. COST's effectiveness was determined by assessing oxidative stress markers, interleukin levels, and histopathological examinations.

Results: Oxidative stress markers were elevated in the ovarian TD group compared to the sham group. COST treatment represented a decline compared to the TD group. Besides, the antioxidant activity was significantly higher in the ovarian TD group than in the sham group. COST treatment improved the antioxidant parameters compared to the TD group. Inflammatory parameters, such as tumour necrosis factor- alpha (TNF-α) and interleukin 1-beta (IL-1β) were higher in the ovarian TD group than the sham group.

Conclusion: COST treatment suppressed the proinflammatory cytokine expression compared to the TD group. Histopathological data supported these findings.

在卵巢扭转/剥离模型中有效抑制氧化损伤、细胞凋亡和自噬的药物--Costunolide。
目的:本研究评估了Costunolide(COST)对卵巢扭转/剥离(TD)模型中氧化组织损伤的疗效:动物被随机分配到假组、卵巢扭转/剥离组、COST 5 mg/kg +卵巢扭转/剥离组和COST 10 mg/kg +卵巢扭转/剥离组。通过评估氧化应激标记物、白细胞介素水平和组织病理学检查来确定 COST 的有效性:结果:与假组相比,卵巢TD组的氧化应激标记物升高。与假组相比,COST治疗组的氧化应激指标有所下降。此外,卵巢TD组的抗氧化活性明显高于假体组。与TD组相比,COST治疗改善了抗氧化参数。卵巢TD组的肿瘤坏死因子α(TNF-α)和白细胞介素1-β(IL-1β)等炎症指标高于假体组:结论:与TD组相比,COST治疗抑制了促炎细胞因子的表达。组织病理学数据证实了这些发现。
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来源期刊
Archives of Physiology and Biochemistry
Archives of Physiology and Biochemistry ENDOCRINOLOGY & METABOLISM-PHYSIOLOGY
CiteScore
6.90
自引率
3.30%
发文量
21
期刊介绍: Archives of Physiology and Biochemistry: The Journal of Metabolic Diseases is an international peer-reviewed journal which has been relaunched to meet the increasing demand for integrated publication on molecular, biochemical and cellular aspects of metabolic diseases, as well as clinical and therapeutic strategies for their treatment. It publishes full-length original articles, rapid papers, reviews and mini-reviews on selected topics. It is the overall goal of the journal to disseminate novel approaches to an improved understanding of major metabolic disorders. The scope encompasses all topics related to the molecular and cellular pathophysiology of metabolic diseases like obesity, type 2 diabetes and the metabolic syndrome, and their associated complications. Clinical studies are considered as an integral part of the Journal and should be related to one of the following topics: -Dysregulation of hormone receptors and signal transduction -Contribution of gene variants and gene regulatory processes -Impairment of intermediary metabolism at the cellular level -Secretion and metabolism of peptides and other factors that mediate cellular crosstalk -Therapeutic strategies for managing metabolic diseases Special issues dedicated to topics in the field will be published regularly.
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