Abstract

Background Perilipin 5 (Plin5) acts as a pivotal mediator of oxidative stress and inflammation and is associated with the progression of relevant diseases. Cerebral ischemic stroke is a severe pathological condition that involves excess oxidative stress and inflammation. However, whether Plin5 plays a role in the progression of cerebral ischemic stroke remains unaddressed. This work focused on the investigation of Plin5 in oxygen-glucose deprivation/reoxygenation (OGD/R)-injured neurons, an in vitro model for studying cerebral ischemic stroke. Methods The primary neuronal cells were isolated from the hippocampus of newborn mice. Neurons were subjected to OGD/R treatment to establish an in vitro model for studying cerebral ischemic stroke. Neurons were infected with recombinant adenovirus expressing Plin5 to upregulate Plin5 expression. The mRNA levels were measured by real-time quantitative PCR (RT-qPCR). Protein levels were determined by immunoblotting. Cell viability was assessed via cell counting kit-8 (CCK-8) assay. Cell apoptosis was evaluated via terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) and Annexin V-Allophycocyanin/7-Amino Actinomycin D (Annexin V-APC/7-AAD) apoptotic assays. Oxidative stress was monitored by dichlorofluorescein diacetate (DCFH-DA) probe. Inflammatory cytokine release was detected by enzyme-linked immunosorbent assay (ELISA). Results A decreased level of Plin5 was observed in neurons challenged with OGD/R. Plin5 overexpression remarkably subdued OGD/R-elicited apoptosis, oxidative stress and proinflammatory response. Plin5 overexpression led to an enhancement of the nuclear factor erythroid 2-related factor 2 (Nrf2) pathway associated with regulation of the Akt-glycogen synthase kinase-3β (GSK-3β). The blocking of Akt was able to reverse the enhancing effect of Plin5 on Nrf2 activation. The restraining of Akt or silencing of Nrf2 diminished the protective effects of Plin5 in OGD/R-injured neurons. Conclusions