■马拉硫磷(MAL),一种使用了几十年的杀虫剂,是一种剧毒物质.一些研究已经记录了这些药物对生殖器官生理的负面影响,但其诱导卵巢功能障碍的确切作用机制尚不清楚.因此,这项研究的目的是研究抗氧化剂橙皮苷(HES)对马拉硫磷引起的卵巢损伤和毒性的影响。
■在本实验中,40只体重27-30g的成年雌性灯泡/c小鼠分为四组,即橙皮苷(20mg/kg,i.p.),马拉硫磷(3mg/kg,i.p.),马拉硫磷+橙皮苷,和对照组。经过连续35天的治疗,小鼠被安乐死,他们的卵巢组织通过H&E染色进行组织病理学分析,通过增殖细胞核抗原(PCNA)和卵泡刺激素受体(FSHR)免疫染色进行免疫组织化学评估,通过测量丙二醛(MDA)水平进行生化评估,超氧化物歧化酶(SOD),过氧化氢酶(CAT),肿瘤坏死因子-α(TNF-α),白细胞介素-1β(IL-1β)。此外,从小鼠血液中收集血清样本进行激素分析,特别是17β-雌二醇(E2),孕酮(P4),黄体生成素(LH),和卵泡刺激素(FSH)。
■结果表明,MAL暴露导致卵巢的体系结构和结构发生异常。此外,用MAL治疗小鼠导致所有三个阶段的卵泡计数下降,即,小学,次要,和第三级,降低血清性激素水平,FSHR和PCNA的免疫反应性降低,CAT和SOD酶活性降低。相比之下,它导致了MDA的增加,IL-1β,和TNF-α,以及闭锁卵泡的计数。尽管如此,观察到HES在所有上述参数中表现出改善马拉硫磷有害影响的能力。
■通过上调PCNA和FSHR的蛋白表达和激活抗氧化防御,用HES治疗能够改善MAL对卵巢组织的不利影响。
UNASSIGNED: Malathion (MAL), a pesticide used for decades, is a highly toxic substance. Several studies have documented the negative effects of such agents on reproductive organ physiology, but the precise mechanism of action in the induction of ovarian dysfunction remains unclear. Therefore, the purpose of this research was to examine the effects of the antioxidant hesperidin (HES) on ovarian damage and toxicity caused by malathion.
UNASSIGNED: In this experiment, forty adult female bulb/c mice weighing 27-30 g were categorized into four groups, namely hesperidin (20 mg/kg, i.p.), malathion (3 mg/kg, i.p.), malathion + hesperidin, and control groups. Following a period of 35 consecutive days of treatment, mice were euthanized, and their ovarian tissues were gathered for the purposes of histopathological analysis by H&E staining, immunohistochemical assessment via proliferating cell nuclear antigen (PCNA) and follicle-stimulating hormone receptor (
FSHR) immunostaining, and biochemical evaluation via measuring the levels of malondialdehyde (MDA), superoxide dismutase (SOD), catalase (CAT), tumor necrosis factor-alpha (TNF-α), and interleukin-1 beta (IL-1β). In addition, serum samples were collected from the blood of mice to perform hormonal analyses, especially 17β-estradiol (E2), progesterone (P4), luteinizing hormone (LH), and follicle-stimulating hormone (FSH).
UNASSIGNED: The results demonstrated that MAL exposure resulted in the development of abnormalities in the architecture and structure of ovaries. Also, the treatment of mice with MAL led to declined follicular counts at all three stages, namely, primary, secondary, and tertiary, reduced serum levels of sex hormones, decreased immunoreactivity of
FSHR and PCNA, and diminished activity of CAT and SOD enzymes. In contrast, it caused an increase in MDA, IL-1β, and TNF-α, as well as the count of atretic follicles. Nonetheless, it was observed that HES exhibited the ability to ameliorate the deleterious impacts of malathion across all the aforementioned parameters.
UNASSIGNED: Treatment with HES via upregulating the protein expression of PCNA and
FSHR and activating antioxidant defense was able to ameliorate the adverse effects of MAL on ovarian tissues.