Effect and Mechanism of Vitexin on the Recovery of Cells After Glucose and Oxygen Deprivation Based on Endoplasmic Reticulum Stress

OBJECTIVE  To investigate the regulation of vitexin on inflammatory factors of oxygen glucose deprivation/re-oxygenation(OGD/R) SH-SY5Y cells and PC12 cells through endoplasmic reticulum stress-related pathways, and to clarify the protective mechanism of vitexin on cells against OGD/R injury.

METHODS  OGD/R-induced SH-SY5Y cell and PC12 cell models were established. They were divided into control group, model group(OGD/R), OGD/R+0.01 µmol·L⁻¹ vitexin group, OGD/R+0.1 µmol·L⁻¹ vitexin group and OGD/R+1 µmol·L⁻¹ vitexin group. CCK-8 assay was performed to evaluate the impact on cell viability. Flow cytometry was used to measure the level of reactive oxygen species(ROS). Immunofluorescence was used to detect the expression of myelin basic protein(MBP). PCR was performed to measure the mRNA levels of endoplasmic reticulum stress-related genes GRP78 and CHOP, as well as the expression levels of inflammatory factors IL-6 and TNF-α. Western blotting was conducted to detect the expression of endoplasmic reticulum stress-related proteins GRP78, ATF6, ATF4, and CHOP.

RESULTS 1 µmol·L⁻¹ vitexin significantly increased cell viability(P<0.05), reduced ROS levels(P<0.01), and increased the expression level of MBP protein(P<0.01). It inhibited the expression of endoplasmic reticulum stress-related proteins GRP78, ATF6, ATF4, and CHOP, and decreased the mRNA levels of endoplasmic reticulum stress-related genes GRP78 and CHOP. It also reduced the levels of inflammatory cytokines IL-6 and TNF-α.

CONCLUSION  In SH-SY5Y cells and PC12 cells, a certain dose of vitexin can effectively inhibite ROS production, promote MBP expression, alleviate the inflammatory injury caused by endoplasmic reticulum stress of damaged nerve cells, and play a certain neuroprotective role.