Iwasa Takeshi, Matsuzaki Toshiya, Yano Kiyohito, Mayila Yiliyasi, Irahara Minoru
Department of Obstetrics and Gynecology, Institute of Biomedical Sciences, Tokushima University Graduate School, 3-18-15 Kuramoto-Cho, Tokushima, 770-8503, Japan.
Department of Obstetrics and Gynecology, Institute of Biomedical Sciences, Tokushima University Graduate School, 3-18-15 Kuramoto-Cho, Tokushima, 770-8503, Japan.
Int J Dev Neurosci. 2018 Oct;69:39-43. doi: 10.1016/j.ijdevneu.2018.06.010. Epub 2018 Jun 30.
Prenatal undernutrition affects some physiological functions after birth, and such changes are associated with the pathogenesis of various diseases. Recently, we have reported that prenatally undernourished male rats exhibited stronger febrile and anorectic responses to immune stress induced by moderate-dose lipopolysaccharide (LPS) treatment in adulthood. In the present study, we evaluated the effects of prenatal undernutrition on stress responses to the administration of a septic dose (3 mg/kg) of LPS in later life, mainly focusing on changes in hypothalamic proinflammatory cytokine expression. We also evaluated the expression of hypothalamic and peripheral reproductive factors because it has been suggested that the stress responses of reproductive functions are affected by prenatal and neonatal stress and nutritional conditions. As a result, we found that prenatal undernutrition attenuated the anorectic response to septic-dose LPS treatment in adulthood in male rats. In addition, it attenuated the LPS-induced suppression of serum testosterone levels and the changes in hypothalamic proinflammatory cytokine (interleukin (IL)-1β, tumor necrosis factor-α, and IL-6) expression induced by septic-dose LPS treatment in adulthood. These results suggest that prenatal undernutrition attenuates stress and reproductive responses under severe immune stress conditions. The downregulation of hypothalamic stress-related factor expression might be involved in such attenuated stress responses, which could be one of the protective mechanisms used to prevent excessive immune responses and aid survival.
产前营养不良会影响出生后的一些生理功能，且这些变化与多种疾病的发病机制相关。最近，我们报道了产前营养不良的雄性大鼠在成年后对中等剂量脂多糖（LPS）治疗诱导的免疫应激表现出更强的发热和厌食反应。在本研究中，我们评估了产前营养不良对后期给予败血症剂量（3 mg/kg）LPS的应激反应的影响，主要关注下丘脑促炎细胞因子表达的变化。我们还评估了下丘脑和外周生殖因子的表达，因为有研究表明生殖功能的应激反应受产前和新生儿期应激及营养状况的影响。结果发现，产前营养不良减弱了成年雄性大鼠对败血症剂量LPS治疗的厌食反应。此外，它还减弱了LPS诱导的成年期血清睾酮水平的抑制以及败血症剂量LPS治疗诱导的下丘脑促炎细胞因子（白细胞介素（IL）-1β、肿瘤坏死因子-α和IL-6）表达的变化。这些结果表明，产前营养不良会减弱严重免疫应激条件下的应激和生殖反应。下丘脑应激相关因子表达的下调可能参与了这种减弱的应激反应，这可能是预防过度免疫反应和促进生存的保护机制之一。
