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缺氧气虚大鼠NEI网络共同化学信号分子变化规律及通心络干预作用
袁国强1,吴以岭1*,贾振华2,吴士珍2,朱慧明2,李娟2
0 字体:加大+\|默认\|缩小-
(1.河北医科大学附属以岭医院络病室,石家庄 050091;2.河北以岭医药研究院络病实验室,石家庄 050035)

摘要:

目的:探讨缺氧气虚大鼠NEI网络共同化学信号分子变化规律及通心络(超微粉碎)的干预影响。方法:Wistar雄性大鼠45只,随机分为3组:空白对照组、气虚模型组、通心络组,每组15只。前两组大鼠按10 ml/kg给予CMCNa灌胃,1次/d；通心络组大鼠按10 ml/kg给予通心络(超微粉碎,1.2 g生药/kg)灌胃,1次/d；气虚模型组与通心络组大鼠灌胃后置于常压低氧舱内,每天7 h,每周6 d,共计5周。实验结束后观察大鼠的生物学表征、进行动脉血气分析、双抗夹心ELISA法测定血清去甲肾上腺素、肾上腺素、5羟色胺(5HT)、多巴胺(DA)、IFNγ的含量,放免法测定皮质酮、三碘甲状腺原氨酸、甲状腺素、IL1β、TNFα水平。放免法测定下丘脑促肾上腺皮质激素释放激素及垂体促甲状腺皮质激素、促肾上腺皮质激素含量；ELISA法测定下丘脑促甲状腺素释放激素含量。结果:与空白对照组比较,气虚模型组大鼠生物学表征评分明显增高(P<0.01),动脉血PaO2显著降低(P<0.05)；血清5HT、DA释放减少(P<0.01)；下丘脑垂体肾上腺(HPA)轴与下丘脑垂体甲状腺(HPT)轴兴奋；血清NE及E释放减少(P<0.01),交感肾上腺髓质系统抑制；IL1β、IFNγ、TNFα等免疫调节因子释放增加(P<0.01)。通心络可明显降低模型大鼠生物学表征评分,升高血氧分压,增加5HT、DA释放、抑制HPA轴与HPT轴的兴奋、降低IL1β、IFNγ水平。结论:采用常压慢性缺氧方法可成功制备气虚大鼠模型。模型大鼠NEI调控网络处于紊乱失衡状态,这可能是缺氧气虚证候产生的重要病生理学基础之一；通心络可增强大鼠耐缺氧能力,改善气虚证候,其机制与调节整体NEI网络失衡有关。

关键词: 缺氧气虚下丘脑垂体系统通心络

DOI：10.3724/SP.J.1008.2008.00787

投稿时间：2007-12-05修订日期：2008-05-06

基金项目:国家重点基础研究发展计划(“973”计划，2005CB523301).

Changes in common chemical signal molecules of neuroendocrine immune network and intervention of Tongxinluo in rats under hypoxia qi asthenia condition

YUAN Guoqiang1,WU Yiling1*,JIA Zhenhua2,WU Shizhen2,ZHU Huiming2,LI Juan2

(1.Department of Luo Diseases,Yiling Hospital Affiliated to Hebei Medical University,Shijiazhuang 050091,China;2.Lab of Luo Diseases of Yiling Medical Research Institute of Hebei Province,Shijiazhuang 050035)

Abstract:

Objective:To investigate the changes in common chemical signal molecules of neuroendocrineimmune (NEI) network and intervention of Tongxinluo (TXL,ultramicropulverization) of rats under hypoxia qiasthenia condition.Methods: Fortyfive male Wistar rats were randomly assigned to the following groups:control group,qiasthenia model group and TXL group (n=15).The rats in the former 2 groups were gavaged with CMCNa (10 ml/kg) once daily; those in the TXL group were gavaged with TXL (ultramicropulverization) suspended in CMCNa (10 ml/kg) once daily.After gavage,animals in the qiasthenia model group and TXL group were placed in a cabin with normal pressure hypoxia (7 h daily,6 d weekly for 5 weeks).At the end of the experiment,the biological characters of rats were observed and arterial blood gas was analyzed.The serum contents of serotonin (5HT),norepinephrine (NE),epinephrine (E),dopamine (DA) and IFNγ and TRH level in the hypothalamus were examined by enzyme linked immunosorbent assay (ELISA); the serum contents of corticosterone (Cort),T3,T4,IL1β,TNFα, and corticotropin release hormone(CRH) in the hypothalamus,and adrenocorticotropic hormone/thyroid stimulating hormone(ACTH/TSH) in the hypophysis cerebri were examined using radioimmunity method.Results: Compared with control group,the biological character scores of rats in the qiasthenia model group were significantly higher(P<0.01),arterial partial pressure of oxygen was significantly lower(P<0.05),the contents of 5HT,DA,NE and E were significantly decreased(P<0.01),the HPA and HPT systems were excited;adrenergic nerveadrenal medulla system was restrained and the release of IL1β,IFNγ and TNFα was significantly increased(P<0.01).The TXL could obviously decrease the biological character score and increase the arterial partial pressure of oxygen in model rats,raise 5HT and DA levels,restrain HPA and HPT system excitation,and decrease IL1β and IFNγ levels.Conclusion: The qiasthenia model can be successfully established using normal pressure chronic hypoxia.The NEI network regulation is chaotic and in a disequilibrium state,which might be an important basis for hypoxia qiasthenia syndrome.TXL can enhance the hypoxia tolerant capability of model rats and improve their qiasthenia syndrome,probably through adjusting NEI network disequilibrium.

Key words: anoxia qi deficiency hypothalamo hypophyseal system Tongxinluo