参二醇组皂苷对内毒素休克大鼠心肌AQP1表达水平的影响

J4 ›› 2010, Vol. 36 ›› Issue (6): 1030-1034.

参二醇组皂苷对内毒素休克大鼠心肌AQP1表达水平的影响

陈晗^1,2, 刘艳波^1,3, 梁作文¹, 邵晨¹, 刘喜春¹, 张键¹, 赵丽晶¹, 赵雪俭¹

(1.吉林大学基础医学院病理生理学教研室|吉林长春 130021；2. 南方医科大学珠江医院|广东广州 510515；3. 北华大学基础医学院病理生理学教研室|吉林吉林 132013）

收稿日期:2010-05-06 出版日期:2010-11-28 发布日期:2010-11-28
通讯作者: 赵丽晶 E-mail:（Tel: 0431-85632348,E-mail: zhao_lj@jlu.edu.cn）
作者简介:陈晗（1985-）|女|吉林省长春市人|在读医学博士|主要从事心肌病理生理学研究。
基金资助:
国家自然科学基金资助课题（30670825）

Effect of panaxadiol saponin on AQP1 expression level in myocardium |of rats with endotoxic shock

CHEN Han^1,2, LIU Yan-Bo^1,3, LIANG Zuo-Wen¹, SHAO Chen¹, LIU Xi-Chun¹, ZHANG Jian¹, ZHAO Li-Jing¹, ZHAO Xue-Jian¹

(1. Department of Pathophysiology,School of Basic Medical Sciences,Jilin University,Changchun 130021,China;2. Zhujiang Hospital,Southern Medical University,Guangzhou 510515,China;3. Department of Pathophysiology,School of Basic Medical Sciences,Beihua University,Jilin 132013,China)

Received:2010-05-06 Online:2010-11-28 Published:2010-11-28

摘要/Abstract

摘要：

目的：探讨人参二醇组皂苷(PDS)对内毒素休克大鼠心肌的保护作用，并揭示其保护作用与水通道蛋白1（AQP1）表达的关系。方法：40只Wistar大鼠分为空白对照组（CTR）、模型组(LPS)、地塞米松组(DEX)及PDS组。LPS（5 mg·kg-1）舌下静脉注射复制内毒素休克模型，监测大鼠平均动脉压（MAP）及动脉压下降的百分数，测量休克240 min大鼠血清天冬氨酸氨基转移酶(AST)、肌酸激酶(CK)和乳酸脱氢酶(LDH)含量及心肌组织匀浆超氧化物歧化酶(SOD)活性和丙二醛(MDA)含量的变化，Western blotting方法检测心肌组织AQP1表达情况。结果：以血压下降至基础血压(0 min)的2/3判定为休克状态，注射LPS5 min　后各组动物均进入休克状态，20 min后平均动脉压（MAP）代偿性回升，于休克第60 min时，LPS组MAP进行性下降，而PDS和DEX组MAP维持稳定而持久的代偿变化；休克240 min时，PDS和DEX组血清AST、CK和LDH含量显著低于LPS组（P<0.05），心肌组织匀浆SOD活性高于LPS组（P<0.05），MDA含量低于LPS组（P<0.05）。Western blotting结果显示：与CTR组比较，LPS组AQP1表达显著降低(P<0.05)，PDS组和DEX组AQP1表达水平明显高于LPS组（P<0.05）。结论：PDS对内毒素休克大鼠心肌具有保护作用，其机制可能是通过增强内毒素血症时心肌毛细血管内皮细胞AQP1蛋白表达，抑制心肌间质水肿而发挥作用。

关键词: 人参二醇组皂苷；内毒素性休克；心肌细胞；水通道蛋白1

Abstract:

To study the protective effect of paraxadiol saponins(PDS) on myocardium of rats with endotoxic shock and reveal the relationship between the protective effect and AQP1 expression level. Methods 40 Wistar rats were divided into 4 groups: control group(CTR),lipopolysaccharide endotoxic shock model group(LPS),dexamethasone treatment group(DEX) and PDS group. LPS (5 mg·kg-1) was administered sublingually to build up the model of endotoxic shock,the mean arterial pressure(MAP) and the decreasing percentage of MAP were monitored at different time. The contents of AST,CK and LDH in serum and SOD activity and MDA content in myocardium were detected after shock for 240 min.The AQP1 expression level in myocardium was detected with Western blotting. Results When the blood pressure fell to 2/3 of the baseline it was regarded as the start of shock. It was found by dynamic observation that the rats entered into shock state at 5 min,the MAP had an compensatory restoration at 20 min,the MAP fell progressively since 60 min until the models got close to death at 240 min in LPS group,but the MAP remained steady and constant compensatory changes in PDS and DEX groups until the rats were sacrificed at 240 min. The serum contents of AST,CK and LDH in LPS group were highest among groups,but in PDS and DEX groups they were lower (P<0.05)；the SOD activities in PDS and DEX groups were higher than those in LPS group (P<0.05),meanwhile the contents of MDA were lower than those in LPS group(P<0.05). Western blotting result showed that the quantity of expression in LPS group was significantly lower than that in control group(P<0.05),but in PDS group and DEX group they were higher than that in LPS group(P<0.05). Conclusion PDS has the protective effect against myocardium injury in rats with endotoxic shock,the mechanism may be adopted to enhance the expression of AQP1 in capillary endothelial cells of LPS-induced endotoxic shock rats,and inhibit the myocardial stromal edema.

Key words: panaxadiol saponin;endotoxic shock;myocardium;aquaporin 1

中图分类号:

R285.5

陈晗, 刘艳波, 梁作文, 邵晨, 刘喜春, 张键, 赵丽晶, 赵雪俭. 参二醇组皂苷对内毒素休克大鼠心肌AQP1表达水平的影响[J]. J4, 2010, 36(6): 1030-1034.

CHEN Han, LIU Yan-Bo, LIANG Zuo-Wen, SHAO Chen, LIU Xi-Chun, ZHANG Jian, ZHAO Li-Jing, ZHAO Xue-Jian. Effect of panaxadiol saponin on AQP1 expression level in myocardium |of rats with endotoxic shock[J]. J4, 2010, 36(6): 1030-1034.

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