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Lipopolysaccharide-induced mechanisms of ovarian dysfunction in cows with uterine inflammatory diseases
Journal of Reproduction and Development ( IF 1.9 ) Pub Date : 2020-01-01 , DOI: 10.1262/jrd.2020-021
Fumie Magata 1
Affiliation  

Uterine inflammatory diseases commonly occur in postpartum dairy cows, resulting in reduced reproductive performance due to aberrant uterine and ovarian activity. Infection of the uterus with gram-negative bacteria results in the detection of lipopolysaccharide (LPS) in the plasma and follicular fluid of cows along with uterine inflammation. LPS acts on follicular components such as theca cells, granulosa cells, and follicle-enclosed oocytes, leading to impaired follicular activity. Follicles with a high LPS environment exhibit reduced follicular steroidogenesis due to the inhibition of steroidogenic enzyme transcription. Primary cell cultures of bovine granulosa and theca cells have shown that LPS acts on follicular cells to impair steroid production, which may disturb follicle growth and/or reduce their ability to ovulate. Even if ovulation occurs, cows with uterine inflammation are less likely to conceive because in addition to uterine damage, LPS also impairs the developmental competence of oocytes. LPS perturbs the nuclear and cytoplasmic maturation of bovine oocytes. Moreover, oocytes matured using LPS treatment are less likely to develop into the blastocyst stage. Such oocytes also have a reduced number of trophoblast cells in blastocysts. Therefore, the detrimental effects of LPS on ovarian activity may be partly responsible for infertility in cows with uterine inflammation. Novel treatment and prevention strategies for uterine inflammatory diseases can be developed by advancing our knowledge of the pathophysiology underlying ovarian dysfunction, and this can only be achieved by further research. The present review outlines the molecular pathogenesis of LPS-induced ovarian dysfunction.

中文翻译:

脂多糖诱导奶牛子宫炎症性疾病卵巢功能障碍的机制

子宫炎性疾病通常发生在产后奶牛中,由于子宫和卵巢活动异常导致繁殖性能下降。革兰氏阴性菌感染子宫导致在奶牛的血浆和卵泡液中检测到脂多糖 (LPS) 以及子宫炎症。LPS 作用于卵泡成分,如卵泡细胞、颗粒细胞和卵泡包裹的卵母细胞,导致卵泡活性受损。由于类固醇生成酶转录的抑制,具有高 LPS 环境的卵泡表现出减少的卵泡类固醇生成。牛颗粒细胞和卵泡膜细胞的原代细胞培养表明,LPS 作用于卵泡细胞以损害类固醇的产生,这可能会干扰卵泡的生长和/或降低它们的排卵能力。即使发生排卵,患有子宫炎症的奶牛也不太可能怀孕,因为除了子宫损伤外,LPS 还会损害卵母细胞的发育能力。LPS 干扰牛卵母细胞的核和细胞质成熟。此外,使用 LPS 处理成熟的卵母细胞不太可能发育到囊胚阶段。这种卵母细胞在囊胚中的滋养层细胞数量也减少。因此,LPS 对卵巢活动的不利影响可能是子宫发炎奶牛不孕的部分原因。通过提高我们对卵巢功能障碍病理生理学的认识,可以开发出治疗和预防子宫炎性疾病的新策略,而这只能通过进一步的研究来实现。
更新日期:2020-01-01
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