Effect of Ginsenoside Rg1 on Apoptosis after Spinal Cord Ischemia-reperfusion Injury in Rats
10.3969/j.issn.1006-9771.2016.06.006
- VernacularTitle:人参皂苷Rg1对大鼠脊髓缺血再灌注损伤后细胞凋亡的影响
- Author:
Fengtao LI
;
Lei LIN
;
Bin CHENG
- Publication Type:Journal Article
- Keywords:
spinal cord injury;
ischemia-reperfusion injury;
ginsenoside Rg1;
apoptosis;
rats
- From:
Chinese Journal of Rehabilitation Theory and Practice
2016;22(6):650-654
- CountryChina
- Language:Chinese
-
Abstract:
Objective To investigate the effect of ginsenoside Rg1 on apoptosis after spinal cord ischemia-reperfusion injury (SCII) in rats. Methods Forty-eight adult Sprague-Dawley rats were randomly divided into sham group (n=8), ischemia group (n=8), ischemia-reper-fusion group (n=16) and drug group (n=16). Fogarty catheter was put in the thoracic aorta of the rats and the blood flow wasn't blocked in the sham group. The rats in the ischemia group were sacrificed 30 minutes after spinal cord ischemia. The drug group was injected with gin-senoside Rg1 30 mg/kg 30 minutes before and after SCII. The same volume of normal saline was injected in the ischemia-reperfusion group at the same time. The expression of Bcl-2 and survivin was detected with immunohistochemistry at six hours, 24 hours after reperfusion in the ischemia-reperfusion group and drug group, 30 minutes after ischemia in the ischemia group and in the sham group. The change of cells was observed in each group with HE staining. Results The cells were damaged in the ischemia group, the ischemia-reperfusion group and the drug group, in which the drug group was better than the other groups. The expression of survivin and Bcl-2 was higher in the ischemia group, the ischemia-reperfusion group and the drug group than in the sham group (t>3.896, P<0.01), and were significantly higher six hours and 24 hours after reperfusion in the drug group than in the reperfusion group (t>6.693, P<0.001). Conclusion Ginsenoside Rg1 can reduce the neurons damage and increase the expression of the Bcl-2 and survivin, that inhibit cells apoptosis after SCII in rats.
