β-HB inhibits the apoptosis of high glucose-treated astrocytes via activation of CREB/BDNF axis

Abstract

ABSTRACT Objective Nerve damage can cause severe limb dysfunction and even leave a lifelong disability. The apoptosis of astrocytes may contribute to the nerve damage. In this research, we sought to investigate the effect of β-HB on nerve damage in vitro. Design Astrocytes were treated with high glucose (HG) to mimic in vitro model of nerve damage. RT-qPCR and western blot were used to detect expressions of CREB, BDNF, Ki-67, PCNA, Bax, Bcl-2 and cleaved caspase 3 in astrocytes, respectively. MTT was used to measure the cell viability. In addition, flow cytometry was used to detect the cell apoptosis. Results β-HB significantly promoted the proliferation and inhibited apoptosis in HG-treated astrocytes. Results showed that of PCNA and Bcl-2 were upregulated, and Bax and cleaved caspase 3 were downregulated after β-HB stimulated in HG-treated astrocytes. In addition, HG-induced inhibition on BDNF expression in astrocytes was notably reversed by β-HB. Furthermore, β-HB promoted the growth and inhibited apoptosis of high glucose-treated astrocytes via activation of CREB/BDNF axis. Conclusion β-HB promotes the growth and inhibits the apoptosis of high glucose-treated astrocytes via activation of CREB/BDNF axis, which may serve as a new target for treatment of nerve damage.