Chen Ming, Chen Zhi-Wu, Long Zi-Jiang, Liu Jin-Lin, Gao Hua-Wu, Wang Ya-Juan
Department of Pharmacology, Anhui University of Traditional Chinese Medicine, Hefei 230038, China.
Zhongguo Zhong Yao Za Zhi. 2013 Apr;38(7):1030-5.
To investigate the effects of sapindus saponins on myocardial inflammation mediated by Ang II/ p38MAPK signal pathway and cardiac hypertrophy in spontaneously hypertensive rats. And also to explore the correlation of cardiac hypertrophy and inflammation.
Thirty-two 16-week-old spontaneously hypertensive rats (SHR) were randomly divided into four groups, one with placebo as model group, one with captopril tablets (27 mg x kg(-1)) as positive control, one with low-dose sapindus saponins (27 mg x kg(-1)), one with high-dose (108 mg x kg(-1)). And another eight healthy Wistar-Kyoto strain (WKY) rats were used as the normal group. The animals were treated for eight weeks, and the indicators detected were as follows: (1) left ventricular mass index (LVMI); (2) the content of Ang II and hs-CRP in plasma were determined by ELISA; (3) the protein expression of AT1R and VEGF were determined by immunohistochemical method; (4) the protein expression of p-p38MAPK in myocardial cells was determined by Western blot.
Sapindus saponins reduced LVMI, and blocked the expression level of Ang II, AT1R, p-p38MAPK, VEGF and hs-CRP in myocardial tissue. Vs the SHR model group, there were significant differences (P < 0.05 or P < 0.01).
Our findings suggested that sapindus saponins could inhibited cardiac hypertrophy, the possible mechanisms may be related to the inhibition on inflammatory response mediated by Ang II/p38MAPK pathway.
探讨无患子皂苷对自发性高血压大鼠中由血管紧张素II/p38丝裂原活化蛋白激酶信号通路介导的心肌炎症及心脏肥大的影响。并探究心脏肥大与炎症之间的相关性。
将32只16周龄的自发性高血压大鼠（SHR）随机分为四组，一组给予安慰剂作为模型组，一组给予卡托普利片（27mg·kg⁻¹）作为阳性对照组，一组给予低剂量无患子皂苷（27mg·kg⁻¹），一组给予高剂量（108mg·kg⁻¹）。另外8只健康的Wistar-Kyoto品系（WKY）大鼠作为正常组。对动物进行为期8周的治疗，检测的指标如下：（1）左心室质量指数（LVMI）；（2）采用酶联免疫吸附测定法测定血浆中血管紧张素II和超敏C反应蛋白的含量；（3）采用免疫组织化学方法测定AT1R和VEGF的蛋白表达；（4）采用蛋白质免疫印迹法测定心肌细胞中p-p38MAPK的蛋白表达。
无患子皂苷降低了LVMI，并阻断了心肌组织中血管紧张素II、AT1R、p-p38MAPK、VEGF和超敏C反应蛋白的表达水平。与SHR模型组相比，差异有统计学意义（P<0.05或P<0.01）。
我们的研究结果表明，无患子皂苷可以抑制心脏肥大，其可能的机制可能与抑制血管紧张素II/p38丝裂原活化蛋白激酶途径介导的炎症反应有关。
