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乌贼墨新型多糖对环磷酰胺致卵巢衰竭小鼠的预防作用及其作用机制。

Preventive Effects of a Novel Polysaccharide from Sepia esculenta Ink on Ovarian Failure and Its Action Mechanisms in Cyclophosphamide-Treated Mice.

机构信息

College of Sciences, Guangdong Ocean University , Zhanjiang 524088, China.

Science Experiment Center, Guilin Medical University , Guilin 541004, China.

出版信息

J Agric Food Chem. 2016 Jul 20;64(28):5759-66. doi: 10.1021/acs.jafc.6b01854. Epub 2016 Jul 6.

DOI:10.1021/acs.jafc.6b01854
PMID:27337058
Abstract

On the basis of our findings about chemo-preventive roles of squid ink polysaccharide and the well-known toxicity of cyclophosphamide (CP) on female gonad, this research investigated the protective effects of a novel polysaccharide from Sepia esculenta ink (SEP) on the ovarian failure resulting from CP, as well as the action mechanisms underpinning this. The results indicated that CP destroyed the ovaries of mice which caused depletion of various follicles, and led to a reduction in estradiol content, increases in FSH and LH contents in sera, decreases in ovary and uterus masses and their relative mass ratios, disruption of the ultrastructure of granulosa cells, as well as induction of apoptosis and autophagy via p38 MAPK and PI3K/Akt signaling pathways. The phenomenon resulted in ovarian failure. However, SEP exposure altered the negative effects completely. The data indicated that SEP can effectively prevent ovarian failure CP caused in mice by inhibiting the p38 MAPK signaling pathway and activating the PI3K/Akt signaling pathway as regulated by CP. SEP was a novel polysaccharide from Sepia esculenta ink with a unique primary structure mainly composed of GalN and Ara that accounted for almost half of all monosaccharides: their ratio was nearly one-to-one. Besides, the polysaccharide contained a small number of Fuc and tiny amounts of Man, GlcN, GlcA, and GalA.

摘要

基于我们对鱿鱼墨多糖的化学预防作用以及环磷酰胺(CP)对女性性腺毒性的发现,本研究调查了来自乌贼墨的新型多糖(SEP)对 CP 引起的卵巢衰竭的保护作用,以及其潜在的作用机制。结果表明,CP 破坏了小鼠的卵巢,导致各种卵泡耗竭,并导致雌二醇含量降低,血清中 FSH 和 LH 含量增加,卵巢和子宫质量及其相对质量比降低,颗粒细胞超微结构破坏,以及通过 p38 MAPK 和 PI3K/Akt 信号通路诱导细胞凋亡和自噬。这种现象导致了卵巢衰竭。然而,SEP 的暴露完全改变了这种负面影响。数据表明,SEP 可以通过抑制 p38 MAPK 信号通路和激活 CP 调节的 PI3K/Akt 信号通路,有效预防 CP 引起的小鼠卵巢衰竭。SEP 是一种来自乌贼墨的新型多糖,具有独特的一级结构,主要由 GalN 和 Ara 组成,几乎占所有单糖的一半:它们的比例接近一比一。此外,该多糖还含有少量的 Fuc 和微量的 Man、GlcN、GlcA 和 GalA。

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