沙打旺素-IV能挽救大鼠颗粒细胞在体外由邻苯二甲酸二(2-乙基己基)酯(DEHP)诱导的氧化应激。

IF 3.3 4区 医学 Q2 REPRODUCTIVE BIOLOGY Reproductive toxicology Pub Date : 2024-10-26 DOI:10.1016/j.reprotox.2024.108737
Vivek Pandey, Alka Sharma, Sonal Upadhayay, Yashvant Patel, Jayhind Kumar Chauhan, Safiya Ayesha, Alakh N Sahu, Rashmi Gupta, Anima Tripathi, Pawan K Dubey
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引用次数: 0

摘要

研究表明,氧化应激(OS)介导的活性氧(ROS)会干扰生殖健康。我们在之前发表的文章中指出,接触邻苯二甲酸二(2-乙基己基)酯(DEHP)会诱发 OS 介导的 ROS 生成,从而抑制类固醇的合成。在本研究中,我们证明了从天门冬根中分离出的一种甾体皂甙(即 Shatavarin-IV)对 DEHP 诱导的大鼠颗粒细胞 OS 的改善/保护作用。大鼠颗粒细胞分别与单独的 DEHP(400μM)、单独的 Shatavarin-IV(8μg/ml)和 DEHP + Shatavarin-IV 组合(400μM + 8μg/ml)体外接触 24 小时。对细胞内 ROS、OS/缺氧、线粒体膜电位、类固醇反应基因的表达进行了分析。结果表明,与对照组相比,有效剂量的 DEHP(400µg)可通过增加 ROS 水平、线粒体膜电位和 β-半乳糖苷酶活性显著增加 OS,并在 mRNA 水平上增加凋亡基因(Bax、Caspase-3)的表达。此外,DEHP 能明显(p
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Shatavarin-IV rescues the Di (2-ethylhexyl) phthalate (DEHP) induced oxidative stress in rat granulosa cells in vitro.

Studies provide notable evidence that oxidative stress (OS) mediated reactive oxygen species (ROS) disturb reproductive health. We have shown in our previous publication that exposure of Di-(2-ethylhexyl) phthalate (DEHP), induces OS mediated ROS generation which inhibits steroid synthesis. In the present study, we demonstrated the ameliorative/protective effects of one of the steroidal saponins, i.e., Shatavarin-IV, isolated from the roots of Asparagus racemosus against DEHP induced OS in rat granulosa cells. Granulosa cells were exposed with DEHP alone (400μM), Shatavarin-IV alone (8μg/ml), and a combination of DEHP + Shatavarin-IV (400μM + 8μg/ml) in vitro for 24 hrs. Intracellular ROS, OS/hypoxia, mitochondrial membrane potential, steroid-responsive genes expression were analyzed. The results revealed that the effective dose of DEHP (400µg) significantly increased OS compared to the control by increasing ROS levels, mitochondrial membrane potential, and β-galactosidase activity with a higher level of apoptotic genes (Bax, Caspase-3) expression at mRNA level. Further, DEHP significantly (p<0.05) reduced mRNA expression of steroidogenic responsive genes (StAR, CYP17A1 and CYP19A1) in granulosa cells treated with above combination compared to control. Interestingly, co-treatment of DEHP + Shatavarin-IV significantly suppressed the DEHP induced OS, ROS, β-galactosidase levels and enhanced steroidogeneic and apoptotic gene expression activities, which suggests that Shatavarin-IV rescued DEHP-induced changes that may useful for the prevention of DEHP- induced reproductive toxicity.

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来源期刊
Reproductive toxicology
Reproductive toxicology 生物-毒理学
CiteScore
6.50
自引率
3.00%
发文量
131
审稿时长
45 days
期刊介绍: Drawing from a large number of disciplines, Reproductive Toxicology publishes timely, original research on the influence of chemical and physical agents on reproduction. Written by and for obstetricians, pediatricians, embryologists, teratologists, geneticists, toxicologists, andrologists, and others interested in detecting potential reproductive hazards, the journal is a forum for communication among researchers and practitioners. Articles focus on the application of in vitro, animal and clinical research to the practice of clinical medicine. All aspects of reproduction are within the scope of Reproductive Toxicology, including the formation and maturation of male and female gametes, sexual function, the events surrounding the fusion of gametes and the development of the fertilized ovum, nourishment and transport of the conceptus within the genital tract, implantation, embryogenesis, intrauterine growth, placentation and placental function, parturition, lactation and neonatal survival. Adverse reproductive effects in males will be considered as significant as adverse effects occurring in females. To provide a balanced presentation of approaches, equal emphasis will be given to clinical and animal or in vitro work. Typical end points that will be studied by contributors include infertility, sexual dysfunction, spontaneous abortion, malformations, abnormal histogenesis, stillbirth, intrauterine growth retardation, prematurity, behavioral abnormalities, and perinatal mortality.
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