Neural Regeneration Research ›› 2014, Vol. 9 ›› Issue (18): 1678-1687.doi: 10.4103/1673-5374.141802

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Ginsenoside Rd inhibits apoptosis following spinal cord ischemia/reperfusion injury

Baogang Wang 1, Qingsan Zhu 2, Xiaxia Man 3, Li Guo 4, Liming Hao 5   

  1. 1 Department of Cardiac Surgery, First Hospital of Jilin University, Changchun, Jilin Province, China
    2 Department of Orthopedics, China-Japan Union Hospital of Jilin University, Changchun, Jilin Province, China
    3 Department of Oncological Gynecology, First Hospital of Jilin University, Changchun, Jilin Province, China
    4 Department of Toxicology, School of Public Health, Jilin University, Changchun, Jilin Province, China
    5 Department of Histology and Embryology, College of Basic Medical Sciences, Jilin University, Changchun, Jilin Province, China
  • Received:2014-08-22 Online:2014-09-26 Published:2014-09-26
  • Contact: Qingsan Zhu, Ph.D., Department of Orthopedics, China-Japan Union Hospital of Jilin University, Changchun 130033, Jilin Province, China, drzqs@yahoo.com.cn.
  • Supported by:

    This study was financially supported by a grant from the Jilin Provincial Science and Technology Development Program Foundation of China, No. 20110915.

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Abstract:

Ginsenoside Rd has a clear neuroprotective effect against ischemic stroke. We aimed to verify the neuroprotective effect of ginsenoside Rd in spinal cord ischemia/reperfusion injury and explore its anti-apoptotic mechanisms. We established a spinal cord ischemia/reperfusion injury model in rats through the occlusion of the abdominal aorta below the level of the renal artery for 1 hour. Successfully established models were injected intraperitoneally with 6.25, 12.5, 25 or 50 mg/kg per day ginsenoside Rd. Spinal cord morphology was observed at 1, 3, 5 and 7 days after spinal cord ischemia/reperfusion injury. Intraperitoneal injection of ginsenoside Rd in ischemia/reperfusion injury rats not only improved hindlimb motor function and the morphology of motor neurons in the anterior horn of the spinal cord, but it also reduced neuronal apoptosis. The optimal dose of ginsenoside Rd was 25 mg/kg per day and the optimal time point was 5 days after ischemia/reperfusion. Immunohistochemistry and western blot analysis showed ginsenoside Rd dose-dependently inhibited expression of pro-apoptotic Caspase 3 and down-regulated the expression of the apoptotic proteins ASK1 and JNK in the spinal cord of rats with spinal cord ischemia/reperfusion injury. These findings indicate that ginsenoside Rd exerts neuroprotective effects against spinal cord ischemia/reperfusion injury and the underlying mechanisms are achieved through the inhibition of ASK1-JNK pathway and the down-regulation of Caspase 3 expression.

Key words: nerve regeneration, spinal cord injury, ginsenoside Rd, ischemia/reperfusion injury, apoptosis, ASK1, JNK, Caspase 3, neural regeneration