精准医学杂志 (Aug 2024)

Protective effect of dihydromyricetin against hippocampal neuronal injury caused by iron overload and its mechanism

  • SUI Yunjie, MA Zegang

DOI
https://doi.org/10.13362/j.jpmed.202404006
Journal volume & issue
Vol. 39, no. 4
pp. 309 – 313

Abstract

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Objective To investigate the protective effect of dihydromyricetin (DMY) against injury of primary hip-pocampal neurons caused by ferric ammonium citrate (FAC) and its mechanism. Methods Primary hippocampal neurons were collected from 24-hour neonatal Sprague-Dawley rats for in vitro culture, and CCK-8 assay was used to measure the viability of primary hippocampal neurons treated with different concentrations of DMY and determine the administration concentration of DMY. Primary hippocampal neurons were divided into control group (H group), 100 mmol/L DMY treatment group (I group), 250 mmol/L FAC treatment group (J group), and 100 mmol/L DMY+250 mmol/L FAC treatment group (K group). Flow cytometry was used to measure the content of reactive oxygen species (ROS) in each group; colorimetry was used to measure the content of malondialdehyde (MDA) in each group; Western blot was used to measure the protein expression levels of nuclear factor erythroid 2-related factor 2 (Nrf2), heme oxygenase-1 (HO-1), and glutathione peroxidase 4 (GPX4) in each group. Results CCK-8 assay showed the highest viability of primary hippocampal neurons at the concentration of 100 mmol/L for DMY (F=9.95,P<0.05), and therefore, this concentration was used for subsequent experiments. Compared with the H group, the J group had significant increases in the content of ROS and MDA (F=176.81,5 523.35,P<0.05), and compared with the J group, the K group had significant reductions in the content of ROS and MDA (F=18.21,412.96,P<0.05). Compared with the H group, the J group had significant reductions in the relative protein expression levels of Nrf2, HO-1, and GPX4 (F=27.35-81.32,P<0.05), and compared with the J group, the K group had significant increases in the relative protein expression levels of Nrf2, HO-1, and GPX4 (F=8.74-21.46,P<0.05). Conclusion DMY can alleviate oxidative stress damage in primary hippocampal neurons due to iron overload, possibly by activating the Nrf2-HO-1/GPX 4 pathway in primary hippocampal neurons.

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