Β-HB inhibits the apoptosis of high glucose-treated astrocytes via activation of CREB/BDNF axis. (24th August 2021)

• Record Type: Journal Article
• Authors: Zhang, Lei; Dong, Da-Long; Gao, Jun-Hong; Wang, An-Kui; Shao, Yong-Ping
• Is Part Of: Brain injury. Volume 35:Number 10(2021)
• Page Start: 1201
• Page End: 1209
• Publication Date: 2021-08-24
• Subjects: β-HB -- nerve damage -- astrocytes -- CREB/BDNF axis; Brain damage -- Periodicals; Brain -- Wounds and injuries -- Periodicals; Brain Injuries -- Periodicals; 617.481
• DOI: 10.1080/02699052.2021.1959061
• Languages: English
• ISSNs: 0269-9052

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.