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

摘要

目的：探索人参皂苷Rg1对于大鼠脊髓缺血再灌注损伤(SCII)后细胞凋亡的影响。方法成年健康Sprague-Dawley大鼠48只，随机分为假手术组(n=8)、缺血组(n=8)、再灌注组(n=16只)和药物组(n=16)。假手术组仅安放球囊不阻断血流；缺血组脊髓缺血30 min；药物组大鼠分别于脊髓缺血前30 min及术后腹腔注射人参皂苷Rg130 mg/kg；再灌注组与药物组相同时间点注射相同体积生理盐水。假手术组、缺血组于缺血后30 min，药物组和再灌注组于再灌注后6 h及24 h应用HE染色检测细胞形态改变，应用免疫组织化学染色检测Bcl-2及survivin表达。结果缺血组、再灌注组及药物组HE染色均有神经元损伤，药物组损伤较其他两组明显减轻。缺血组、再灌注组和药物组survivin、Bcl-2阳性细胞明显高于假手术组(t>3.896, P<0.01)。药物组6 h、24 h survivin及Bcl-2蛋白阳性细胞均较再灌注组显著增加(t>6.693, P<0.001)。结论人参皂苷Rg1可减少早期大鼠SCII后神经元损害，增加抗凋亡蛋白survivin、Bcl-2的表达，抑制凋亡。%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.