4.0 Article

Neuroprotective effect of neuregulin-1β on spinal cord ischemia reperfusion injury

Journal

JOURNAL OF SPINAL CORD MEDICINE
Volume 44, Issue 4, Pages 583-589

Publisher

TAYLOR & FRANCIS LTD
DOI: 10.1080/10790268.2019.1600837

Keywords

Neuregulin; Spinal cord injury; Ischemia reperfusion; Matrix metalloproteinases-9; Tissue inhibitor of metalloproteinase-1

Funding

  1. Science & Technology Fund of Tianjin Municipal Commission of Health and Family Planning [KZ025]

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NRG-1 beta reduced the damage of SCII in rats by decreasing the expression of MMP-9 and increasing the expression of TIMP-1, suggesting its protective role in spinal cord ischemia and reperfusion injury.
Objective: This study was designed to see if neuregulin-1 beta (NRG-1 beta) plays a protective role in spinal cord ischemia and reperfusion injury (SCII). Design: Animal research. Setting: China. Participants: NA. Interventions: Forty-eight SD rats were randomly divided into control group (n=16), SCII model group (n=16) and NRG-1 beta -treated group (n=16). In control group, the abdominal aorta was isolated but not clipped. The rats in NRG-1 beta -treated group were treated with 10 mu g/kg NRG-1 beta during developing SCII model. Outcome Measures: Neurological scores were evaluated. At 3, 6, 12 and 24h after the reperfusion, rats were killed. Pathological changes of spinal cord were assessed with HE staining, and immunohistochemical staining of matrix metalloproteinases-9 (MMP-9) and tissue inhibitor of metalloproteinase-1 (TIMP-1). MMP-9 and TIMP-1 mRNA levels were assessed using real-time PCR. Results: NRG-1 beta reduced the damage of SCII in the rats. The expression of MMP-9 protein and mRNA in NRG-1 beta treatment group was significantly lower than the model group (P<0.05) at 6h, 12h and 24h after the perfusion. The expression of TIMP-1 protein and mRNA in the treatment group was significantly higher than the model group at 12h and 24h after the perfusion. Conclusion: NRG-1 reduced the reperfusion damage in rat model of SCII, in which process MMP-9 and TIMP-1 were probably involved.

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