人参皂苷Rb1通过减轻线粒体损伤对大鼠脊髓缺血再灌注损伤的保护作用

doi:10.3969/j.issn.1006-9771.2018.06.002

Abstract

Abstract: Objective To observe the effects of ginsenoside Rb1 pretreatment on spinal cord ischemia-reperfusion injury in rats, and to explore the possible mitochondrial mechanism of ginsenoside Rb1 against ischemia-reperfusion injury. Methods The spinal cord ischemia-reperfusion injury model was established. The rats were randomly divided into sham operation group (n=12), ischemia-reperfusion group (n=12) and drug group (n=12). The drug group received ginsenoside Rb1 peritoneal injection with 10 mg/kg, 20 mg/kg, 40 mg/kg and 80 mg/kg, respectively, 30 minutes before modeling and once a day after modeling. After 48 hours of reperfusion, the BBB score was tested, the levels of superoxide dismutase (SOD) and malonaldehyde (MDA) in the serum and spinal cord tissue, and the cytochrome C oxidase (COX) activity in spinal cord tissue were detected.Results Compared with the ischemia-reperfusion group, the BBB score increased (P<0.05), the SOD level increased, and the MDA level decreased both in serum and spinal cord tissue, the activity of COX increased in the spinal cord tissue (P<0.05). All the indexes were dose-dependent, however, no difference was found between 40 mg/kg and 80 mg/kg.Conclusion Ginsenoside Rb1 can inhibit oxidative stress induced by spinal cord ischemia-reperfusion injury in rats by inhibiting mitochondrial damage. The protective effect of ginsenoside Rb1 on the spinal cord ischemia-reperfusion injury is dose-dependent during 10 to 40 mg/kg dose.

Key words: spinal cord injury, ischemia-reperfusion, ginsenoside Rg1, mitochondria, rats

CLC Number:

R651.2

CHENG Bin, YANG Feng, LI Feng-tao, LIN Lei, XUE Jian-li, WU Hao, YE Jin-tao. Protective Effect of Ginsenoside Rb1 on Spinal Cord Ischemic-reperfusion Injury in Rats by Alleviating Mitochondrial Damage[J]. 《Chinese Journal of Rehabilitation Theory and Practice》, 2018, 24(6): 629-633.

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Protective Effect of Ginsenoside Rb1 on Spinal Cord Ischemic-reperfusion Injury in Rats by Alleviating Mitochondrial Damage

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