Background To investigate the effect of a novel brain-derived peptide HIBDAP (Hypoxic Ischemic Brain Damage Associated Peptide) on cell apoptosis after oxygen-glucose deprivation (OGD) in PC12 cells.Methods The sequence of HIBDAP (HSQFIGYPITLFVEKER) was coupled with the carrier peptide of the transactivator of transcription (TAT) sequence (YGRKKRRQRRR). The FITC labeled TAT-HIBDAP was observed by the uorescence microscope. After TAT-HIBDAP treatment and OGD treatment, PC12 cell apoptosis rate was analyzed using lactate dehydrogenase (LDH) leakage andAnnexin V-uorescein isothiocyanate (FITC) assay. Mitochondrial membrane potential (ΔΨm) assay was examined by uorescence microscope. Protein expressions of apoptosis factors were examined by Western blotting.Results FITC-labelled TAT-HIBDAP could enter into PC12 cell nucleus. Compared with the OGD group, TAT-HIBDAP at low concentrations (1μM, 5μM, 10μM) signi cantly reduced the apoptosis rate of PC12 cells except the 20μM concentration, especially the 5μM concentration has the most obvious effect. There were remarkable increases of △Ψm after different concentrations (1μM, 5μM, 10μM, 20μM) of TAT-HIBDAP pretreatment and the 5μM concentration also has the most obvious effect. TAT-HIBDAP could rescue the increased ratio of Bax/Bcl-2 and Caspase-3 activation induced by OGD.Conclusions TAT-HIBDAP is resistance to OGD-induced PC12 cells apoptosis through regulating the pathway of Bax/Bcl-2/Caspase-3, which may supply a novel therapeutic strategy for neonatal HIBD.

Background To investigate the effect of a novel brain-derived peptide HIBDAP (Hypoxic Ischemic Brain Damage Associated Peptide) on cell apoptosis after oxygen-glucose deprivation (OGD) in PC12 cells. Methods The sequence of HIBDAP (HSQFIGYPITLFVEKER) was coupled with the carrier peptide of the transactivator of transcription (TAT) sequence (YGRKKRRQRRR). The FITC labeled TAT-HIBDAP was observed by the fluorescence microscope. After TAT-HIBDAP treatment and OGD treatment, PC12 cell apoptosis rate was analyzed using lactate dehydrogenase (LDH) leakage andAnnexin V-fluorescein isothiocyanate (FITC) assay. Mitochondrial membrane potential (ΔΨm) assay was examined by fluorescence microscope. Protein expressions of apoptosis factors were examined by Western blotting. Results FITC-labelled TAT-HIBDAP could enter into PC12 cell nucleus. Compared with the OGD group, TAT-HIBDAP at low concentrations (1μM, 5μM, 10μM) significantly reduced the apoptosis rate of PC12 cells except the 20μM concentration, especially the 5μM concentration has the most obvious effect. There were remarkable increases of △Ψm after different concentrations (1μM, 5μM, 10μM, 20μM) of TAT-HIBDAP pretreatment and the 5μM concentration also has the most obvious effect. TAT-HIBDAP could rescue the increased ratio of Bax/Bcl-2 and Caspase-3 activation induced by OGD. Conclusions TAT-HIBDAP is resistance to OGD-induced PC12 cells apoptosis through regulating the pathway of Bax/Bcl-2/Caspase-3, which may supply a novel therapeutic strategy for neonatal HIBD.