| 张健,张瑞光,蔡茜,等.参芪扶正注射液对放射性脑损伤保护的分子机制探讨[J].中华放射医学与防护杂志,2015,35(6):419-422.Zhang Jian,Zhang Ruiguang,Cai Qian,et al.Shenqi Fuzheng Injection (SFI) inhibits irradiation-induced brain injury[J].Chin J Radiol Med Prot,2015,35(6):419-422 |
| 参芪扶正注射液对放射性脑损伤保护的分子机制探讨 |
| Shenqi Fuzheng Injection (SFI) inhibits irradiation-induced brain injury |
| 投稿时间：2014-10-16 |
| DOI：10.3760/cma.j.issn.0254-5098.2015.06.004 |
| 中文关键词: 参芪扶正注射液 急性放射性脑损伤 炎性因子 小胶质细胞激活 NF-κB |
| 英文关键词:Shengqi Fuzheng injection Irradiation induced acute brain injury Inflammatory factors Microglia activation NF-κB |
| 基金项目:国家自然科学基金(30800283,81172595);中国博士后科学基金(20100480905);中国临床肿瘤学科学基金(Y-L2011-002) |
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| 中文摘要: |
| 目的 研究参芪扶正注射液对于放疗引起脑损伤保护的分子机制。方法 将6~8周龄C57BL/6J小鼠按随机数字表法随机分成3组:空白对照组:不做任何处理;单纯照射组:全脑照射20 Gy;照射加药组:全脑20 Gy照射后参芪扶正注射液(20 mg/kg)治疗4周;水迷宫检测参芪扶正注射液对放射性脑损伤后小鼠认知功能的影响;Real-time PCR检测急性脑损伤后炎性因子TNF-α与IL-1β表达情况;免疫荧光检测急性放射性脑损伤后海马区的小胶质细胞的激活水平;免疫荧光检测各组NF-κB p65的胞质胞核表达水平。结果 Morris水迷宫显示,参芪扶正注射液可以改善小鼠放射性脑损伤后的认知功能障碍(t=6.34、6.70,P<0.05);PCR显示照射后TNF-α在3 h表达最高,随后下降,在4周又达到较高水平,参芪扶正注射液治疗下调TNF-α表达水平(t=11.34、9.70、6.07,P<0.05);IL-1β在照射后表达水平逐渐升高,在72 h达到较高水平,其后开始下降,而参芪扶正注射液可以降低照射后IL-1β表达水平(t=12.27、5.70、7.52,P<0.05);免疫荧光显示参芪扶正注射液能够抑制海马区小胶质细胞激活(t=12.35、8.64、7.82,P<0.05);小胶质细胞p65免疫荧光显示参芪扶正注射液照射后NF-κB p65胞质、胞核的转位。结论 参芪扶正注射液可能通过抑制NF-κB p65的胞质、胞核转位,抑制小胶质细胞的激活,从而下调炎性因子的表达,起到治疗放射性脑损伤的作用。 |
| 英文摘要: |
| Objective To explore the effect of SFI in radiation-induced mice brain injury after 20 Gy cranial radiation. Methods The mice were divided into three groups: (1) control group,(2) RT-only group:the whole brain was irradiated with a dose of 20 Gy, (3) RT and SFI group: SFI at 20 ml/kg/d from 4 weeks after 20 Gy cranial radiation theraty(CRT). Results Morris water maze test showed that the latency of the irradiated group was longer than control group and SFI improved the cognitive function of mice(t=6.34,6.70,P<0.05). The expression of TNF-α reached to the highest level at 3 h after irradiation, and then it decreased but got the second higher level again at 4 weeks after irradiation. The expression of IL-1β reached to the highest level at 72 h after irradiation and decreased until 4 weeks after irradiation. SFI decreased both expressions of TNF-α(t=11.34,9.70,6.07,P<0.05)and IL-1β(t=12.27,5.70,7.52,P<0.05). Immune florescence staining showed that SFI reduced the number of activated microglia(t=12.35,8.64,7.82,P<0.05)and inhibited the translocation of p65 of microglia after irradiation. Conclusions Findings suggest that SFI may decrease microglial activation and suppress the expression of TNF-α and IL-1β by inhibiting the translocation of NF-κB p65 and then attenuate irradiation-induced brain injury. |
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