Background/Objective:
Grape seed proanthocyanidins (GSPs) are a group of polyphenolic
bioflavonoids, which possess a variety of biological functions and pharmacological properties. We
studied the neuroprotective effects of GSP against oxygen-glucose deprivation/reoxygenation
(OGD/R) injury and the potential mechanisms in mouse neuroblastoma N2a cells.
Methods:
OGD/R was conducted in N2a cells. Cell viability was evaluated by CCK-8 and LDH release
assay. Apoptosis was assessed by TUNEL staining and flow cytometry. Protein levels of cleaved
caspase-3, Bax and Bcl-2 were detected by Western blotting. CHOP, GRP78 and caspase-12 mRNA
levels were assessed by real-time PCR. JC-1 dying was used to detect mitochondrial membrane potential.
ROS levels, activities of endogenous antioxidant enzymes and ATP production were examined to
evaluate mitochondrial function.
Results:
GSP increased cell viability after OGD/R injury in a dose-dependent manner. Furthermore,
GSP inhibited cell apoptosis, reduced the mRNA levels of CHOP, GRP78 and caspase-12 (ER stressassociated
genes), restored mitochondrial membrane potential and ATP generation, improved activities
of endogenous anti-oxidant ability (T-AOC, GXH-Px, and SOD), and decreased ROS level.
Conclusion:
Our findings suggest that GSP can protect N2a cells from OGD/R insult. The mechanism
of anti-apoptotic effects of GSP may involve attenuating ER stress and mitochondrial dysfunction.
Grape seed proanthocyanidins reactivate silenced tumor suppressor genes in human skin cancer cells by targeting epigenetic regulators
