Publications by authors named "Ye-Xing Tao"

The aim of this study was to determine the mechanisms driving the protective effects of squid ink polysaccharide (SIP) against cyclophosphamide (CP)-induced testicular damage, focusing on germ cells. In the testes of mice exposed to CP and/or SIP, the present study examined the levels of reactive oxygen species (ROS) and malondialdehyde, activity of superoxide dismutase levels, protein expression levels of B-cell lymphoma 2 (Bcl2), Bcl2-associated X protein (Bax), and total Caspase 3, activation of p-p38 and p-Akt proteins, and tissue morphology. The findings indicated that CP induced ROS production and oxidative stress, resulting in testicular damage.

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In our recent reports, a squid ink polysaccharide (SIP) was found having preventive activity against cyclophosphamide induced damage in mouse testis and ovary. Here we further reveal the regulative mechanism of SIP against chemical toxicity on testis. Leydig cells exposed to acrolein (ACR) underwent apoptosis at 12h and 24h.

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Objectives: This paper aims to investigate synergistic inhibition of polysaccharide from ink (SIP), a newly isolated marine polysaccharide in our laboratory, on breast cancer MDA-MB-231 cells exposed to cisplatin.

Materials And Methods: Cell viability of MDA-MB-231 cells was determined by CCK 8 assay. Median-effect concentration was analyzed using Chou-Talalay method that was also subjected to determine cell inhibition ratio and combined index, as well as interaction between SIP and cisplatin.

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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.

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