脂多糖诱导炎症对小鼠睾丸kisspeptin系统的调节作用

IF 2.8 4区 医学 Q2 REPRODUCTIVE BIOLOGY
Jaldhi , Shweta , Shashank Kumar Maurya , Amrita Bakshi
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引用次数: 0

摘要

Kisspeptin是一种神经肽激素,在调节生殖中起着不可或缺的作用。它作用于促性腺激素释放激素的上游,控制促性腺激素的释放和伴随的性腺功能,反过来又受性腺类固醇激素的调节。然而,kisspeptin (Kiss1)及其受体(Kiss1r)在包括睾丸在内的下丘脑以外的组织中也有表达。由于免疫挑战导致生殖功能受损,目前的工作重点是研究脂多糖(LPS)诱导的炎症对成年小鼠睾丸kisspeptin系统的调节。LPS在体内慢性处理7天,导致精管形状不规则,周长、直径和截面积减小,生精细胞排列扭曲,结缔组织破坏,导致间质空间增大,精子数量减少。此外,睾丸中促炎细胞因子Tnfα的表达水平升高证实了炎症的诱导。在kisspeptin系统中,在基因和蛋白水平上均观察到睾丸Kiss1r的表达显著增加,而Kiss1r的表达则明显减少,这意味着在感染状态下睾丸kisspeptin可能在控制生殖功能方面发挥了代偿作用。此外,我们用LPS体外处理睾丸碎片3 h和6 h,以了解炎症对睾丸kisspeptin系统的直接影响。两个时间点Tnfα表达均升高,Tgfβ1表达均降低。在转录水平上,Kiss1在LPS处理6 h时表达减少,但在3 h时没有变化。Kiss1r在3 h时表达增加,而在6 h时表达减少。在蛋白水平上,两个时间点睾丸Kiss1水平均下降,而Kiss1r无明显变化。因此,本研究证明了脂多糖诱导的炎症对睾丸kisspeptin系统的调节作用。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Lipopolysaccharide-induced inflammation modulates testicular kisspeptin system in mice
Kisspeptin, a neuropeptide hormone, plays an indispensable role in regulating reproduction. Acting upstream of gonadotropin-releasing hormone, it controls gonadotropin release, and concomitant gonadal functions, and in turn, is regulated by gonadal steroid hormones. Nevertheless, expression of kisspeptin (Kiss1) and its receptor (Kiss1r) is reported in tissues other than hypothalamus, including testes. Since immune-challenged conditions lead to compromised reproductive functions, the present work emphasizes on investigating regulation of the testicular kisspeptin system in adult mice by lipopolysaccharide (LPS)-induced inflammation. In vivo chronic treatment of LPS for 7 days caused irregularly-shaped seminiferous tubules with reduced perimeter, diameter and cross-sectional area, distorted arrangement of spermatogenic cells, disrupted connective tissue leading to increased interstitial space and reduced sperm count. Further, elevated expression level of pro-inflammatory cytokine, Tnfα, in the testis validated the induction of inflammation. Regarding the kisspeptin system, a significant increase in testicular Kiss1 but a decrease in Kiss1r expression was observed at both gene and protein levels, implying a possible compensatory role of testicular kisspeptin to control reproductive functions under an infectious state. Further, an in vitro treatment of testicular fragments with LPS was conducted for 3 h and 6 h to understand the direct effect of inflammation on the testicular kisspeptin system. An increased Tnfα but decreased Tgfβ1 expression was observed at both time points. At the transcript level, Kiss1 showed a reduced expression at 6 h but no change at 3 h of LPS treatment. Regarding Kiss1r, an increased expression at 3 h but decreased at 6 h was seen. At the protein level, decreased levels of testicular Kiss1 was observed at both the time points while Kiss1r exhibited no significant change. Hence, the present work demonstrated modulation of the testicular kisspeptin system by LPS-induced inflammation.
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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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