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Int J Biol Macromol. 2019 Aug 23;140:1098-1105. doi: 10.1016/j.ijbiomac.2019.08.200. [Epub ahead of print]

Beneficial effect of Sepia esculenta ink polysaccharide on cyclophosphamide-induced immunosuppression and ovarian failure in mice.

Author information

1
College of Chemistry & Environment, Guangdong Ocean University, Zhanjiang 524088, China.
2
College of Agriculture, Guangdong Ocean University, Zhanjiang 524088, China.
3
College of Chemistry & Environment, Guangdong Ocean University, Zhanjiang 524088, China. Electronic address: luopingna@163.com.

Abstract

In order to investigate prevention of squid ink polysaccharide (SIP) against cyclophosphamide (CP) induced ovarian failure and immunosuppression in mice, female Kunming mice were subjected to intraperitoneal injection of CP (120 mg/kg) and oral administration of SIP (50, 65, 80 and 110 mg/kg, continuous 14 days). At the end of the experiment, animals were sacrificed to collect sera, spleens, thymuses and ovaries for determining relative masses of organs, serum hormonal levels, contents of interleukin 2 (IL-2) and tumor necrosis factor α (TNF-α) in ovary and serum, superoxide dismutase (SOD) activity and malonaldehyde (MDA) content in ovary, contents of nuclear factor E2 related factor 2 (Nrf2) signaling pathway-related proteins in ovary, and peripheral blood populations of CD4+, CD8+ and natural killer (NK) cells. Results showed that CP induced immunosuppression in mice which was demonstrated by decreased relative masses of spleen and thymus, contents of IL-2 and TNF-α, ratio of CD4+ / CD8+, and increased population of NK cells. But the suppressive action was disinhibited by SIP. Meanwhile, CP treatment caused dysfunction of ovaries in mice that could be concluded by decreased relative mass of ovary, disruption of redox equilibrium, and modified contents of Nrf2 signaling pathway-related proteins. However, SIP exposure rescued the negative effect CP mediated in ovaries of mice. These data can be concluded that SIP protects mice from CP inducing immunosuppression and ovarian failure via Nrf2/ARE (antioxidant response element) signaling pathway.

KEYWORDS:

Cyclophosphamide; Immunity; Mice; Ovarian failure; SIP

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