Neuroprotective effect of a novel brain-derived peptide, HIBDAP, against oxygen-glucose deprivation through inhibition of apoptosis in PC12 cells

BackgroundThe effect of a novel brain-derived peptide, hypoxic-ischemic brain damage associated peptide (HIBDAP), on apoptosis after oxygen-glucose deprivation (OGD) in PC12 cells was investigated.MethodsThe HIBDAP sequence (HSQFIGYPITLFVEKER) was coupled with the carrier peptide of the transactivator of transcription (TAT) sequence (YGRKKRRQRRR). FITC-labelled TAT-HIBDAP was observed by fluorescence microscopy. After TAT-HIBDAP treatment and OGD treatment, the PC12 cell apoptosis rate was analysed using lactate dehydrogenase (LDH) leakage and Annexin V-fluorescein isothiocyanate (FITC) assays. Mitochondrial membrane potential (Delta psi m) was examined by fluorescence microscopy. Protein expression of apoptotic factors was examined by Western blotting.ResultsFITC-labelled TAT-HIBDAP entered the PC12 cell nucleus. Compared with the OGD group, TAT-HIBDAP at low concentrations (1 mu M, 5 mu M, 10 mu M) significantly reduced the apoptosis rate of PC12 cells (except at 20 mu M); 5 mu M TAT-HIBDAP had the most obvious effect. There were remarkable increases in Delta psi m at different concentrations (1 mu M, 5 mu M, 10 mu M, 20 mu M) of TAT-HIBDAP pretreatment, and 5 mu M TAT-HIBDAP also had the most obvious effect. TAT-HIBDAP reversed the increased ratio of Bax/Bcl-2 and activation of Caspase-3 induced by OGD.ConclusionTAT-HIBDAP is resistant to OGD-induced PC12 cell apoptosis by regulating the Bax/Bcl-2/Caspase-3 pathway, which may provide a novel therapeutic strategy for neonatal HIBD.

Automated summary

This study investigated the effect of a novel brain-derived peptide, HIBDAP, on apoptosis in PC12 cells after OGD. The results showed that TAT-HIBDAP could resist OGD-induced PC12 cell apoptosis by regulating the Bax/Bcl-2/Caspase-3 pathway.