Chen Ming, Chen Zhi-Wu, Long Zi-Jiang, Liu Jin-Lin, Bian Hai, Wang Ya-Juan, Wang Liang
Department of Pharmacology, Anhui University of Traditional Chinese Medicine, Hefei 230038, China.
Zhong Yao Cai. 2013 Feb;36(2):249-55.
To investigate the effect of Sapindus saponins on myocardial inflammation and left ventricular remodeling in spontaneously hypertensive rats.
Forty 16-week-old spontaneously hypertensive rats were randomly divided into five groups, placebo as model group, captopril tablets (27 mg/kg) as positive control, low-dose Sapindus saponins (27 mg/kg), medium-dose (54 mg/ kg) and high-dose (108 mg/kg) groups. And another eight healthy Wistar-Kyoto strain (WKY) rats were used as the normal group. The animals were treated for eight weeks, and the detection indexes were as follows: (1) Calculated left ventricular mass index (LVMI); (2) Observed the morphological changes on left ventricular myocardial tissue by HE staining; (3) Observed the collagen distribution in left ventricular myocardial by Masson staining; (4) Detected the protein expression of TGF-beta1 by immunohistochemical assay.
Sapindus saponins could effectively reverse the left ventricular hypertrophy phenomenon in SHR, lowered LVMI, inhibited the myocardial cell hypertrophy and hyperplasia of collagen fibers, and blocked the expression level of TGF-beta1 in myocardial when compared with the SHR model group, there were significant differences (P < 0.05 or P < 0.01).
Sapindus saponins can reserve the left ventricular remodeling in pathological conditions, its possible mechanism may be related to the inhibition of myocardial tissue inflammation factor of TGF-beta1.
探讨无患子皂苷对自发性高血压大鼠心肌炎症及左心室重构的影响。
将40只16周龄自发性高血压大鼠随机分为五组，以生理盐水为模型组，卡托普利片（27mg/kg）为阳性对照组，低剂量无患子皂苷（27mg/kg）、中剂量（54mg/kg）和高剂量（108mg/kg）组。另取8只健康Wistar-Kyoto品系（WKY）大鼠作为正常组。动物治疗8周，检测指标如下：（1）计算左心室质量指数（LVMI）；（2）通过HE染色观察左心室心肌组织形态学变化；（3）通过Masson染色观察左心室心肌中胶原分布；（4）采用免疫组织化学法检测TGF-β1蛋白表达。
与SHR模型组相比，无患子皂苷能有效逆转SHR左心室肥厚现象，降低LVMI，抑制心肌细胞肥大和胶原纤维增生，并阻断心肌中TGF-β1的表达水平，差异有统计学意义（P<0.05或P<0.01）。
无患子皂苷可在病理状态下逆转左心室重构，其可能机制可能与抑制心肌组织炎症因子TGF-β1有关。
