Effect of Sargassum fusiforme polysaccharides on activating JNK/Nrf2/ARE signaling pathway and slowing down aging process
10.7501/j.issn.0253-2670.2018.23.018
- Author:
Zi-Hui ZHAO
1
Author Information
1. College of Life and Environment Science, Wenzhou University
- Publication Type:Journal Article
- Keywords:
Anti-aging;
Anti-oxidant;
JNK;
Nrf2;
Sargassum fusiforme polysaccharides
- From:
Chinese Traditional and Herbal Drugs
2018;49(23):5600-5609
- CountryChina
- Language:Chinese
-
Abstract:
Objective To study the mechanisms of anti-oxidation and anti-aging of Sargassum fusiforme polysaccharides (SFPS). Methods qRT-PCR and Western blotting were utilized to detect the expression of c-Jun-N-terminal kinase 1/2 (JNK1/2) in male mice with different ages and in the old male mice fed with SFPS. The JNK isoforms were specifically distinguished by RT-PCR and the expression levels of each isoform in the liver of mice by ig administration of SFPS or normal saline were measured. Finally, the mechanism of JNK activating Nrf2/ARE signaling pathway was determined by co-immunoprecipitation and ARE-luciferase reporter gene assay. Results The expression levels of JNK1/2 were negatively correlated with aging process. JNK1-β2, JNK2-α1, and JNK2-β2 played important roles in aging process. The mRNA expression level of JNK1-β2, JNK2-α1, and JNK2-β2 were significantly decreased in mice aging process, and the protein expression levels of JNK1-β2 (5.4×104) were significantly upregulated by long-term diet with SFPS. The JNK1-β2 (5.4×104) protein interacted with anti-oxidant factor Nrf2, and significantly activated Nrf2/ARE signaling pathway. Conclusion JNK1-β2, JNK2-α1 and JNK2-β2 had negative correlation with aging process, and the expression level of JNK1-β2 (5.4×104) in aged mice were obviously promoted by long-term diet with SFPS. As JNK1-β2 containing C-terminal tail can interact with Nrf2 and activate the NRF2/ARE signaling pathway, therefore, it was suggested that SFPS can improve the overall anti-oxidant capacity and retard aging process by activating of the JNK1-β2/Nrf2/ARE signaling pathway.
