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大鼠脂多糖诱导的低体温反应的激素同步。

Hormonal synchronization of lipopolysaccharide-induced hypothermic response in rats.

机构信息

Aksaray University, Faculty of Art and Science, Department of Biology, 68100 Aksaray, Turkey.

出版信息

J Endocrinol Invest. 2013 Nov;36(10):816-24. doi: 10.3275/8945. Epub 2013 Apr 23.

Abstract

BACKGROUND

Recent experimental evidence suggests that lipopolysaccharide (LPS)-induced hypothermia is an adaptive thermoregulatory strategy against immunological challenge in rats. We hypothesized that the hormones which are predominantly responsible for energy homeostasis may have efferent signaling roles for development of the hypothermia.

AIM

The aim of the study was to evaluate the changes of hypothalamic-pituitary-thyroid (HPT) and hypothalamic- pituitary-adrenal (HPA) axis hormones, leptin and erythropoietin at various phases of LPS-induced hypothermia such as the initial phase, nadir and the end of the response in blood sampled rats.

MATERIAL AND METHODS

Body temperature of adult male albino Wistar rats was recorded by biotelemetry. E. coli O111:B4 LPS (250 μg/kg, ip) was injected alone or with SC-560, a cyclooxygenase-1 selective inhibitor (1 mg/kg, sc).

RESULTS

Serum FT4 levels elevated at the initial phase, but FT3 levels decreased at nadir and remained low at the end of the response. Meanwhile, no change was observed in TSH levels. Serum adrenocorticotropic hormone (ACTH) levels reduced at the initial phase and serum corticosterone levels decreased at nadir without any change in serum corticotropin-releasing hormone (CRH) levels throughout the hypothermia. Serum leptin levels increased only at the end of the response. No change was observed in the levels of serum erythropoietin. SC-560 treatment abolished both LPS-induced hypothermia and respective hormonal changes.

CONCLUSION

Data suggest that HPT axis hormones may contribute to development of LPS-induced hypothermia in rats. Data also support the view that leptin may have a role for the recovery of hypothermic response.

摘要

背景

最近的实验证据表明,脂多糖(LPS)诱导的体温降低是大鼠对抗免疫挑战的适应性体温调节策略。我们假设,主要负责能量平衡的激素可能对外周信号传递在体温降低的发展中发挥作用。

目的

本研究旨在评估下丘脑-垂体-甲状腺(HPT)和下丘脑-垂体-肾上腺(HPA)轴激素、瘦素和促红细胞生成素在 LPS 诱导的体温降低的各个阶段(初始阶段、最低点和反应结束时)在血液样本大鼠中的变化。

材料和方法

成年雄性白化 Wistar 大鼠的体温通过生物遥测法记录。单独注射大肠杆菌 O111:B4 LPS(250μg/kg,ip)或注射 COX-1 选择性抑制剂 SC-560(1mg/kg,sc)。

结果

血清 FT4 水平在初始阶段升高,但 FT3 水平在最低点降低,在反应结束时仍保持较低水平。同时,TSH 水平没有变化。血清促肾上腺皮质激素(ACTH)水平在初始阶段降低,血清皮质酮水平在最低点降低,整个体温降低过程中血清促皮质素释放激素(CRH)水平没有变化。血清瘦素水平仅在反应结束时升高。血清促红细胞生成素水平没有变化。SC-560 治疗消除了 LPS 诱导的体温降低和相应的激素变化。

结论

数据表明,HPT 轴激素可能有助于大鼠 LPS 诱导的体温降低的发展。数据还支持瘦素可能在恢复体温降低反应中起作用的观点。

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