2. Academic Validation
  3. Protective Effect of Salidroside on Mitochondrial Disturbances via Reducing Mitophagy and Preserving Mitochondrial Morphology in OGD-induced Neuronal Injury

Protective Effect of Salidroside on Mitochondrial Disturbances via Reducing Mitophagy and Preserving Mitochondrial Morphology in OGD-induced Neuronal Injury

  • Curr Med Sci. 2021 Oct;41(5):936-943. doi: 10.1007/s11596-021-2374-6.
Cai-Ying Hu  # 1,  Qian-Ying Zhang  # 2 3,  Jie-Hui Chen 2,  Bin Wen 2,  Wei-Jian Hang 2 4,  Kai Xu 2,  Juan Chen 5,  Ben-Hong He 6
Affiliations

Affiliations

  • 1 Department of Cardiology, Wuhan Red Cross Hospital, Wuhan, 430015, China.
  • 2 Department of Biochemistry and Molecular Biology, School of Basic Medicine, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430030, China.
  • 3 Department of Clinical Laboratory, Affiliated Wuhan Mental Health Center, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430030, China.
  • 4 Division of Cardiology, Department of Internal Medicine, and Hubei Key Laboratory of Genetics and Molecular Mechanisms of Cardiological Disorders, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430030, China.
  • 5 Department of Biochemistry and Molecular Biology, School of Basic Medicine, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430030, China. chenjuanlinda69@163.com.
  • 6 Department of Cardiovascular Medicine, Lichuan People's Hospital, Lichuan, 445400, China. lczyyhbh@163.com.
  • # Contributed equally.
PMID: 34181207 DOI: 10.1007/s11596-021-2374-6
Abstract

Salidroside is the active ingredient extracted from Rhodiola rosea, and has been reported to show protective effects in cerebral ischemia, but the exact mechanisms of neuronal protective effects are still unrevealed. In this study, the protective effects of salidroside (1 µmol/L) in ameliorating neuronal injuries induced by oxygen-glucose deprivation (OGD), which is a classical model of cerebral ischemia, were clarified. The results showed that after 8 h of OGD, the mouse hippocampal neuronal cell line HT22 cells showed increased cell death, accompanied with mitochondrial fragmentation and augmented Mitophagy. However, the cell viability of HT22 cells showed significant restoration after salidroside treatment. Mitochondrial morphology and mitochondrial function were effectively preserved by salidroside treatment. The protective effects of salidroside were further related to the prevention of mitochondrial over-fission. The results showed that mTOR could be recruited to the mitochondria after salidroside treatment, which might be responsible for inhibiting excessive Mitophagy caused by OGD. Thus, salidroside was shown to play a protective role in reducing neuronal death under OGD by safeguarding mitochondrial function, which may provide evidence for further translational studies of salidroside in ischemic diseases.

Keywords

mTOR; mitochondria quality control; oxygen-glucose deprivation; salidroside.

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