Chinese Journal of Tissue Engineering Research ›› 2020, Vol. 24 ›› Issue (在线): 1-.

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Triptolide improves spinal cord injury recovery via upregulation of autophagy and inhibition of apoptosis in Thy-yfp transgenic mice

Zhu Ning, Yang Xinming, Ruan Jianwei   

  1. First Affiliated Hospital of Hebei North University, Zhangjiakou 075000, Hebei Province, China
  • Received:2019-12-10 Revised:2019-12-14 Accepted:2020-03-03 Online:2020-12-08 Published:2020-05-08
  • Contact: Yang Xinming, MD, Professor, First Affiliated Hospital of Hebei North University, Zhangjiakou 075000, Hebei Province, China
  • About author:Zhu Ning, Master candidate, Physician, First Affiliated Hospital of Hebei North University, Zhangjiakou 075000, Hebei Province, China
  • Supported by:
    2011 Medical Science Research Key Project of Hebei Provincial Department of Health, No. 20110176; 2013 Innovative Talent Cultivation Foundation of Hebei North University, No. CXRC1322

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Abstract:

BACKGROUND: Studies have shown that treatment with triptolide reduces ischemic lesion area, water content, and nerve cell death in a rat model of stroke. In addition, triptolide can promote the repair of spinal cord injury by inhibiting astrocyte hyperplasia, microglia activation and inflammatory response.

OBJECTIVE: To investigate the effect of triptolide on the autophagy and apoptosis in the spinal cord of Thy-YFP transgenic mice after spinal cord injury.

METHODS: Sixty Thy-YFP transgenic mice were randomly divided into four groups: sham, dimethyl sulfoxide (DMSO), triptolide and methylprednisolone groups. Following the establishment of the spinal cord injury models, mice in the triptolide, DMSO and sham group were immediately intraperitoneally injected with triptolide (0.2 mg/kg·d) or 5% DMSO-normal saline solution (0.2 mg/kg·d) for 7 days, whereas mice in the methylprednisolone group were intraperitoneally injected with methylprednisolone (30 mg/kg) at 30 minutes, 6 hours and 24 hours after surgery. BMS score was used to detect the recovery of motor function; hematoxylin-eosin staining and Nissl staining were used to explore tissue recovery after spinal cord injury; western blot and immunofluorescence staining were employed to assess the levels of autophagy-associated proteins, Beclin-1, LC3B, p62, and apoptosis-associated proteins, Bcl-2, Bax and caspase-3. An ethic approval for animal experiments was obtained from Hebei North University with an approval No. W20200002.

RESULTS AND CONCLUSION: Treatments with triptolide or methylprednisolone after spinal cord injury significantly improved motor function and reduced neuronal cell death. In addition, autophagy-associated protein LC3B was upregulated and p62 downregulated following triptolide treatment, apoptosis-associated proteins caspase-3 and Bax were reduced, while anti- apoptosis protein Bcl-2 was increased after triptolide treatment. To conclude, triptolide improves the motor function after spinal cord injury, which is related to upregulation of autophagy and inhibition of apoptosis. Triptolide may be a potential neuroprotective agent for spinal cord injury.

Key words: triptolide, autophagy, apoptosis, spinal cord injury

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