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Alleviating impact of hydroethanolic Murraya koenigii Murraya koenigii leaves extract on bisphenol A instigated testicular lethality and apoptosis in mice

机译:缓解羟乙醇杂船Koenigii Murraya Koenigii叶提取物在双酚中叶提取物溶血睾丸致死性和小鼠凋亡

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Abstract Bisphenol A (BPA) is a well‐known endocrine disruptor that imposees adverse effects on male fertility via interacting with germ cells of testis. Objectives of present study were to investigate the possible protective effects of hydroethanolic Murraya koenigii leaves extract (HEMKLE) against BPA‐induced testicular damage and apoptosis in mice. Male Balb/c mice were divided into four different groups: Group I (control), Group II (HEMKLE), Group III (BPA) and Group IV (HEMKLE?+?BPA). Group III (BPA) showed significant decrease in sperm parameters, germ cell number along with increased lipid peroxidation (LPO) and reactive oxygen species (ROS). A significant decrease in antioxidant enzymes activity was also observed in Group III (BPA) animals. mRNA expression study revealed significant decrease in the expression of Bcl‐2 and increase in expressions of caspase‐9 and caspase‐3, thus clearly demonstrate BPA‐induced apoptosis. In addition, HEMKLE co‐administration to BPA‐treated mice showed a significant increase in sperm parameters, germ cell number, decreased levels of LPO and ROS, increased antioxidant enzymes activity in Group IV (HEMKLE?+?BPA). Also, mRNA expression study showed a significant increase in Bcl‐2 and decrease in caspase‐9 and caspase‐3 gene expressions in Group IV (HEMKLE?+?BPA). Thus, the present study suggests that HEMKLE intervention provides protection against BPA‐induced oxidative stress and apoptosis.
机译:摘要双酚A(BPA)是一种众所周知的内分泌干扰,通过与睾丸的生殖细胞相互作用施加对雄性生育能力的不利影响。目前研究的目的是探讨氢乙醇莫罗萨Koenigii叶子提取物(血管)对小鼠睾丸损伤和细胞凋亡的可能保护作用。将雄性BALB / C小鼠分为四种不同的组:I族(对照),II族(血管),III组(BPA)和IV组(血管α+?BPA)。 III组(BPA)显示精子参数的显着降低,种质细胞数以及增加的脂质过氧化(LPO)和活性氧(ROS)。在III组(BPA)动物中也观察到抗氧化酶活性的显着降低。 mRNA表达研究表明,Bcl-2的表达和Caspase-9和Caspase-3表达的增加显着降低,从而清楚地证明了BPA诱导的细胞凋亡。此外,对BPA处理的小鼠的血管共同给药表现出精子参数,生殖细胞数,LPO和RO水平降低的显着增加,IV组中的抗氧化酶活性增加(血管α+βBA)。此外,mRNA表达研究显示Bcl-2的显着增加,并在IV组中的Caspase-9和Caspase-3基因表达的降低(血管α+βbPa)。因此,本研究表明,血管干预提供了免受BPA诱导的氧化应激和凋亡的保护。

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