摘要
目的:探讨安宫牛黄散中朱砂、雄黄的药理作用机制。方法:SD大鼠随机分成6组(12只／组):正常对照组、外伤性脑水肿膜型对照组、朱砂组(0．15 g/kg)、雄黄组(0．15 g/kg)、安宫牛黄散(下简称整方)组(1．5 g/ kg)、去朱砂、雄黄的安宫牛黄散(下简称拆方)组(1．2 g/kg),以上各组再设8 h分组和24 h分组(6只／分组)。RT-PCR法测定脑组织中热休克蛋白70(HSP70)mRNA表达;比色法测定脑组织中一氧化氮合酶(NOS)及其同工酶(iNOS、cNOS)活力;放免法测定血清中细胞因子TNF-α、IL-1β水平。结果:造模后8 h,整方组与拆方组HSP 70 mRNA表达均较模型组增高(P<0．05),且整方组诱导HSP 70 mRNA表达的作用强于拆方组(P<0．05);朱砂、雄黄、整方和拆方均能降低iNOS活力,且较模型组明显降低(P<0．05),其中整方组抑制作用最为显著。雄黄组、整方组、拆方组TNF-α水平较模型组降低(P<0．05),整方组与拆方组IL-1β水平较模型组降低(P<0．05)。结论: HSP 70、iNOS、TNF-α及IL-β参与了外伤性脑水肿的病理过程。安宫牛黄散和复方中的朱砂、雄黄对外伤性脑水肿大鼠脑组织的保护作用可能与通过增加诱导HSP 70 mRNA表达、抑制iNOS活力和炎症细胞因子TNF-α、IL-1β的生成有关。
Objective： To explore the pharmacological mechanism of Cinnabar and Realgar in Angong Niuhuang powder（ANP）. Methods： SD rats were randomly divided into six groups（ 12 rats/group） ： normal controls group（ NS group）, contusion cerebral edema model group（ CCE group） , cerebral edema rats administrated by cinnabar 0. 15 g/kg 1h（ CA group） , cerebral edema rats administrated by realgar 0. 15 g/kg 1h（ RG group） , cerebral edema rats administrated by Angong Niuhuang powder 1.5 g/kg 1h（ANP Ⅰ group） , cerebral edema rats administrated by Angong Niuhuang powder substracted cinnabar and realgar 1.2 g/kg 1h（ ANP Ⅱ group）. Each group was divided into two subgroups（6 rats/subgroup）. The rats in subgroups were killed at 8h and 24h after modeling respectively. Expression of heat shock protein 70 （ HSP 70 ） mRNA in brain tissues was measured by RT-PCR. Activities of nitric oxide synthase （NOS） and its isoenzymes（ iNOS, eNOS）in brain tissues were tested by eolorimetry. Levels of tumor necrosis factor-α（TNF-α） and inteleukin-1β（ 1L-1β） in serum were determined by radioimmunoassay （RIA）. Resuhs ： Expression of HSP 70 mRNA in ANP Ⅰ group and ANP Ⅱ group significantly increased as compared with CCE group 8h after being modeled（ P 〈0. 05 ）, and increase range in ANP Ⅰ group were singificantly higher than that in ANP Ⅱ group（P 〈0. 05）. Activities of iNOS in CA group, RG group, ANP Ⅰ group and ANP Ⅱ group were lower than that in CCE group 8h after being modeled（ P 〈0. 05）, and the activities in ANP Ⅰ group were the lowest in the four groups. Levels of TNF-α in RG group, ANP Ⅰ group and ANP Ⅱ group decreased obviously as compared with CCE group 8h after being modeled（P 〈 0. 05）, so did levels of IL-1β in ANP Ⅰ group and ANP Ⅱ group（ P 〈0. 05）. But no significant difference was shown between ANP I group and ANP Ⅱ group. Conclusion ： HSP 70, iNOS, TNF-α and IL-1β are involved in contusion cerebral edema. ANP and CA, RG in ANP are protective against CCE in rats. It may be associated with the increase of HSP 70 mRNA expression, inhibition of iNOS activity, and the decreasae of inflammatory cytokines（ TNF-α, IL-1β）levels.
出处
《中药材》
CAS
CSCD
北大核心
2006年第5期458-461,共4页
Journal of Chinese Medicinal Materials
基金
广东省自然科学基金项目(010270)
