4.7 Article

Characterization of PCS-2A, a polysaccharide derived from chestnut shell, and its protective effects against H2O2-induced liver injury in hybrid grouper

Journal

INTERNATIONAL JOURNAL OF BIOLOGICAL MACROMOLECULES
Volume 193, Issue -, Pages 814-822

Publisher

ELSEVIER
DOI: 10.1016/j.ijbiomac.2021.10.185

Keywords

Chestnut shell polysaccharide; Hepatoprotection; Structural characterization; NRF2 molecular pathway

Funding

  1. Heyuan Municipal Science and Technology Project [2019002]

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PCS-2A is an acidic polysaccharide purified from chestnut shell with a molecular weight of 34,023 Da, containing various sugar units in specific ratios. It shows potential in protecting liver cells from H2O2-induced injury through activation of the NRF2 signaling pathway, reducing oxidative stress and inflammatory response.
PCS-2A is a 34,023-Da acidic polysaccharide purified from chestnut shell consisting of rhamnose, arabinose, galactose, glucose, ribose, and galacturonic acid subunits at a molar ratio of 0.019:0.044:0.059:0.052:0.197:0.628. FTIR, methylation, and NMR analyses suggest the following backbone, (-> 4)-alpha-D-GalAp-(1 -> 2,4)-alpha-L-Rha-(1 ->), with the branch chain composed of arabinose on O-2 with 2,4)-alpha-L-Rha-(1 ->). CCK-8 assay indicated PCS-2A treatment offset the reduction in cell viability inflicted by H2O2. Furthermore, histological signs of recovery in hepatocytes and liver tissue and a decreased level of AST and ALT occurred following administration of PCS-2A, indicating anti-liver lesion capability. In addition, we found that PCS-2A effectively alleviated H2O2-induced oxidative stress via activation of the NRF2 signaling pathway, evidenced by the downregulation of ROS content and upregulation of Nrf2 expression, as well as its corresponding antioxidant enzymes. The antioxidative effect elicited by PCS-2A further ameliorated NF-kappa B-mediated inflammation, as evidenced by lower mRNA levels of inflammatory cytokines, higher I kappa B in vitro, and reduced gene expression and activities of proinflammatory cytokines in vivo. Furthermore, in vitro apoptosis-related indicators revealed that P53-mediated apoptosis was alleviated via oxidative stress modulation. In summary, these results suggest that PCS-2A may elicit a protective effect against H2O2-induced liver injury via upregulation of the NRF2 signaling pathway.

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