Polysaccharide from the seeds of Plantago asiatica L. alleviates nonylphenol induced reproductive system injury of male rats via PI3K/Akt/mTOR pathway
[Display omitted] •PLCP protected male rats against NP exposure induced reproductive system injury.•PLCP alleviated histopathologic injury in testis of NP induced rats.•PLCP relieved oxidative damage in testis and epididymis of NP induced rats.•PLCP ameliorated hormone expressions in serum and testi...
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Veröffentlicht in: | Journal of functional foods 2020-03, Vol.66, p.103828, Article 103828 |
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Format: | Artikel |
Sprache: | eng |
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Zusammenfassung: | [Display omitted]
•PLCP protected male rats against NP exposure induced reproductive system injury.•PLCP alleviated histopathologic injury in testis of NP induced rats.•PLCP relieved oxidative damage in testis and epididymis of NP induced rats.•PLCP ameliorated hormone expressions in serum and testis.•PLCP reduced NP-induced apoptosis and autophagy via PI3K/Akt/mTOR pathway.
The preventive role of polysaccharide from the seeds of Plantago asiatica L. (PLCP) against reproductive system injury induced by nonylphenol (NP) was investigated. Male Sprague-Dawley rats were exposed orally to NP 1 h after PLCP intragastric administration continuously for 45 days. The results showed that NP induced significant decrease in relative weight of testes and epididymis, changed testicular histomorphology, and disrupted hormone secretions. Moreover, oxidative stress occurred after NP exposure by overproduction of Malondialdehyde, lipid peroxidation, inducible nitric oxide synthase, and low activities of superoxide dismutase and catalase. Furthermore, the induction of apoptosis and disturbance of PI3K/Akt/mTOR pathway by NP were also proved. Interestingly, PLCP alleviated NP toxicity by improving antioxidant enzymes, recovering hormone secretions, inhibiting apoptosis and autophagy, which involves PI3K/Akt/mTOR pathway. These findings provide a good direction that PLCP may be a good candidate to help body defend against toxic substance, particularly endocrine disrupting chemicals induced reproductive toxicity. |
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ISSN: | 1756-4646 2214-9414 |
DOI: | 10.1016/j.jff.2020.103828 |