β-HB inhibits the apoptosis of high glucose-treated astrocytes via activation of CREB/BDNF axis
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.
| Medienart: |
E-Artikel |
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| Erscheinungsjahr: |
2021 |
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| Erschienen: |
2021 |
| Enthalten in: |
Zur Gesamtaufnahme - volume:35 |
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| Enthalten in: |
Brain injury - 35(2021), 10 vom: 24. Aug., Seite 1201-1209 |
| Sprache: |
Englisch |
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| Beteiligte Personen: |
Zhang, Lei [VerfasserIn] |
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| Links: |
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| Themen: |
β-HB |
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| Anmerkungen: |
Date Completed 11.10.2021 Date Revised 11.10.2021 published: Print-Electronic Citation Status MEDLINE |
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| doi: |
10.1080/02699052.2021.1959061 |
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| funding: |
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| Förderinstitution / Projekttitel: |
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| PPN (Katalog-ID): |
NLM329274686 |
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| 245 | 1 | 0 | |a β-HB inhibits the apoptosis of high glucose-treated astrocytes via activation of CREB/BDNF axis |
| 264 | 1 | |c 2021 | |
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| 500 | |a Date Completed 11.10.2021 | ||
| 500 | |a Date Revised 11.10.2021 | ||
| 500 | |a published: Print-Electronic | ||
| 500 | |a Citation Status MEDLINE | ||
| 520 | |a 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 | ||
| 520 | |a 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 | ||
| 520 | |a 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 | ||
| 520 | |a 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 | ||
| 650 | 4 | |a Journal Article | |
| 650 | 4 | |a Research Support, Non-U.S. Gov't | |
| 650 | 4 | |a CREB/BDNF axis | |
| 650 | 4 | |a astrocytes | |
| 650 | 4 | |a nerve damage | |
| 650 | 4 | |a β-HB | |
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| 700 | 1 | |a Dong, Da-Long |e verfasserin |4 aut | |
| 700 | 1 | |a Gao, Jun-Hong |e verfasserin |4 aut | |
| 700 | 1 | |a Wang, An-Kui |e verfasserin |4 aut | |
| 700 | 1 | |a Shao, Yong-Ping |e verfasserin |4 aut | |
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