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Sinomenine reduces neuronal cell apoptosis in mice after traumatic brain injury via its effect on mitochondrial pathway
Authors Fu C, Wang Q, Zhai X, Gao J
Received 18 October 2017
Accepted for publication 22 November 2017
Published 5 January 2018 Volume 2018:12 Pages 77—84
DOI https://doi.org/10.2147/DDDT.S154391
Checked for plagiarism Yes
Review by Single-blind
Peer reviewer comments 3
Editor who approved publication: Professor Manfred Ogris
Chuanjing Fu,1,* Qi Wang,2 Xiaofu Zhai,3,* Juemin Gao1
1Department of Neurosurgery, Jiangsu Hospital of Traditional Chinese Medicine, Nanjing, 2Department of Radiology, The Fourth People’s Hospital of Huai’an, 3Department of Neurosurgery, The Second People’s Hospital of Huai’an, Xuzhou Medical College, Huai’an, People’s Republic of China
*These authors contributed equally to this work
Background: Sinomenine (SIN) has been shown to have protective effects against brain damage following traumatic brain injury (TBI). However, the mechanisms and its role in these effects remain unclear. This study was conducted to investigate the potential mechanisms of the protective effects of SIN.
Methods: The weight-drop model of TBI in Institute of Cancer Research (ICR) mice were treated with SIN or a vehicle via intraperitoneal administration 30 min after TBI. All mice were euthanized 24 h after TBI and after neurological scoring, a series of tests were performed, including brain water content and neuronal cell death in the cerebral cortex.
Results: The level of cytochrome c (Cyt c), malondialdehyde (MDA), glutathione peroxidase (GPx) and superoxide dismutase 1 (SOD) were restored to some degree following the SIN treatment. The SIN treatment significantly decreased caspase-3 expression and reduced the number of positive cells by terminal deoxynucleotidyl transferase-mediated dUTP nick end-labeling (TUNEL) assay and improved the survival of neuronal cells. Additionally, the pretreatment levels of MDA were restored, while Bax translocation to mitochondria and Cyt c release into the cytosol were reduced by the SIN treatment.
Conclusion: SIN protected neuronal cells by protecting them against apoptosis via mechanisms that involve the mitochondria following TBI.
Keywords: sinomenine, traumatic brain injury, apoptosis, mitochondria
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