天津医药

天津医药 ›› 2015, Vol. 43 ›› Issue (3): 245-248.doi: 10.11958/j.issn.0253-9896.2015.03.006

• 实验研究 • 上一篇    下一篇

人参皂苷 Rg1 对局灶性脑缺血大鼠 PARP-1 和 TNFR1表达的影响

于洋 1， 刘学政 1△， 包翠芬 2， 李晓明 3， 刘霞 3   

  1. 1辽宁医学院解剖学教研室 （邮编 121000） ;2省高校分子细胞生物与新药开发重点实验室； 3组织胚胎学教研室
  • 收稿日期:2014-09-30 修回日期:2014-10-25 出版日期:2015-03-15 发布日期:2015-03-15
  • 通讯作者: 刘学政 E-mail:Liuxuezhengvip@sina.com
  • 作者简介:于洋 （1980）， 女， 硕士在读， 主要从事脑血管疾病防治的基础研究
  • 基金资助:
    国家自然科学基金资助项目 （81202783）； 辽宁省自然科学基金项目 （2014022008）； 辽宁省教育厅一般项目 （LR2013092）

Effects of ginsenoside Rg1 on PARP-1 and TNFR1 expression in rat model of focal cerebral ischemia

YU Yang1, LIU Xuezheng1△, BAO Cuifen2, LI Xiaoming3, LIU Xia3   

  1. 1 Department of Human Anatomy, Liaoning Medical University, Jinzhou 121000, China;2 Key Lab of Molecular Cell Biology and New Drug Development; 3 Histology and Embryolog
  • Received:2014-09-30 Revised:2014-10-25 Published:2015-03-15 Online:2015-03-15
  • Contact: LIU Xuezheng E-mail:Liuxuezhengvip@sina.com

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摘要： 目的 探讨人参皂苷 Rg1 对局灶性脑缺血大脑皮质多聚二磷酸腺苷核糖聚合酶 （PARP） -1 和肿瘤坏死因子受体(TNFR)1 表达的影响。方法 90 只健康 SD 大鼠随机均分为假手术组， 单纯缺血组， 人参皂苷 Rg1 低、 中、 高组， 阳性对照组。于术前 5 d 至取材当日， 假手术组与单纯缺血组分别腹腔注射生理盐水 45 mg/kg， 人参皂苷 Rg1 分别给 10、 20、 40 mg/kg， 阳性对照组尼莫地平 1 mg/kg。采用大脑中动脉栓塞法制备局灶性脑缺血模型， 神经功能缺损评分和 TTC 染色验证模型是否成功； 采用免疫组织化学法和蛋白免疫印迹法检测大脑皮质缺血后 PARP-1、 TNFR1的表达。结果 单纯缺血组较假手术组可见明显神经功能缺陷症状及大面积苍白色梗死区域； 人参皂苷 Rg1 各组和阳性对照组神经功能评分和脑梗死体积百分比高于假手术组， 低于单纯缺血组（P＜0.05）； 人参皂苷 Rg1 各组与阳性对照组差异无统计学意义。人参皂苷 Rg1 低组每高倍视野 PARP-1、 TNFR1 阳性细胞数高于假手术组和阳性对照组； 中、 高组高于假手术组， 低于单纯缺血组 （P＜0.05）。单纯缺血组皮质 PARP-1、 TNFR1 较假手术组阳性表达条带显著增强； 人参皂苷 Rg1 低组 PARP-1、 TNFR1 阳性表达高于假手术组； 中组高于假手术组， 低于单纯缺血组；高组低于单纯缺血组 （P＜0.05）。结论 人参皂苷 Rg1 对大鼠局灶性脑缺血具有保护作用， 其机制可能与下调大脑组织 PARP-1、 TNFR1 的表达， 对抗脑细胞坏死有关。


关键词: 人参皂甙, 脑缺血, 聚 ADP 核糖聚合酶类, 受体, 肿瘤坏死因子, Ⅰ型, 人参皂苷 Rg1, 局灶性脑缺血, PARP-1, TNFR1

Abstract:  Objective To explore effects of ginsenosides Rg1 on the expression of poly(ADP- ribose) polymerase1 (PARP- 1) and tumor necrosis factor receptor (TNFR) 1 in cortex cells after focal cerebral ischemia in rats. Methods Ninety healthy rats were randomly divided into sham-operative group, focal cerebral ischemia group, ginsenoside Rg1groups (low, medium and high concentrations) and drug control group. Rats were intraperitoneally injected saline 45 mg/kg, saline 45 mg/kg+ginsenosides Rg1 10, 20 and 40 mg/kg, nimodipine 1 mg/kg 5 d before surgery, respectively. Focal cerebral ischemia model was made by middle cerebral artery occluding in rats. The neurological deficit score and TTC staining were used to verify the success of the rat model. The expressions of PARP-1 and TNFR1 were evaluated by immunohistochemical method and Western blot technique. Results There were obvious symptoms of neurological deficit and large pale infarct area in focal cerebral ischemia group compared with those of sham-operative group. There were higher percentages of neurological deficit score and infarct area in ginsenosides Rg1 groups and positive control group than those of sham-operative group, but which were lower than those of ischemia group (P＜0.05). There were no significant differences between ginsenosides Rg1 groups and positive control group. The positive cells of PARP- 1 and TNFR1 were higher in ginsenosides Rg1 low- dose group than those of sham-operative group and positive control group, while ones of medium and high-dose Rg1 group were higher than those of sham-operative group, and were lower than those of ischemia group (P＜0.05). Compared with sham-operative group, PARP-1 and TNFR1 expression strips were significantly enhanced in ischemia group. Expression strips were higher in ginsenosides Rg1 low-dose group than those of shamoperative group. Expression strips were higher in ginsenosides Rg1 medium-dose group than those of sham-operative group, but which were lower than those of ischemia group, and ones of high-dose group were lower than ischemia group (P＜0.05). Conclusion Ginsenoside Rg1 shows protective effects on focal ischemia injury, which may be related with down-regulation of the expression of PARP-1 and TNFR1.

Key words: GINSENOSIDE, brain ischemia, poly(ADP-ribose) polymerases, receptors, tumor necrosis factor, type I;ginsenoside Rg1, focal cerebral ischemia, PARP-1, TNFR1