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作 者:周辉[1] 张安平[1] 陈敏珠[1] 徐叔云[1] 汪国良
机构地区:[1]安徽医科大学临床药理研究所
出 处:《中国药理学通报》1994年第6期429-432,共4页Chinese Pharmacological Bulletin
摘 要:本文以血浆皮质酮(CS)、促肾上腺皮质激素(ACTH)和β-内啡肽(β-END)含量为指标,观察了白芍总甙(TGP)对不同状态(正常或不同应激)的大鼠下丘脑-垂体-肾上腺轴(HPAA)及其免疫功能的调节作用。结果表明,TGP对正常大鼠的HPAA呈现小剂量(12.5~50.0mg·kg-1)兴奋(血浆CS含量升高)和大剂量(100~200mg·kg-1)抑制(血浆CS含量降低)的剂量依赖性调节作用。其次,TGP可兴奋轻度应激(20℃水游泳)大鼠的HPAA和抑制重度应激(4℃水游泳或24h束缚)大鼠的HPAA,使过高的血浆CS、ACTH和β-END含量降低,提示TGP对应激大鼠HPAA呈现轴机能依赖性的调节作用。此外,TGP在降低束缚应激大鼠血浆CS、ACTH和β-END水平的同时,上调受抑大鼠脾淋巴细胞ConA增殖反应和腹腔M释放H2O2,提示TGP的免疫调节作用可能与其调节HPAA的功能有关。Total glucosides of paeony TGP either raised the excitability of HPAA (CS level raised) with small doses (12. 5 ̄ 50 mg·kg-1)or depressed the one of HPAA (CS level reduced) with large doses(100 ̄200mg·kg-1), indicating that it played an important role in the dose-dependent modulatory effects in normal rats'HPAA. Under lighter stress (swimming, 20℃, TGP excited the stimulated rat's HPAA. However, under heavier stress (swimming,4℃)it inhibited the over-stim-ulated rat's HPAA, which served as the protection of HPAA from exhaustion.These results show that TGP regulates the HPAA function, depending on the different activation state of this axis in stress rats. In addition TGP upregulated the deficient mitogenisis of T lymphocytes and the dinimished release of hydrogen peroxide from the peritoneal MΦs in restraint-stress rats,as well as down-regulated their elevated CS,ACTH and β-END levels in plasma, indicating that the effect of TGP on immune function relates to its modulatory effect on HPAA.
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