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目的观察棓丙酯(PrG)对异丙肾上腺素(Iso)致大鼠心肌纤维化(MF)的影响,并探讨其可能的作用机制。方法 8周龄雄性SD大鼠50只,随机分为正常对照组、模型组、棓丙酯低剂量组(PrG-L组)、棓丙酯中剂量组(PrG-M组)、棓丙酯高剂量组(PrG-H组),每组10只。背部皮下注射Iso制备MF模型。7d后,PrG-L、PrGM、PrG-H组分别腹腔注射棓丙酯注射液18、36、72mg/kg,正常对照组和模型组按上述相同方法注射等量生理盐水。定期观察大鼠状态、活动、饮食、毛发等一般情况。4周后,检测大鼠心脏血流动力学参数,计算心脏质量指数和左心室质量指数,ELISA试剂盒测定血清中肿瘤坏死因子-α(TNF-α)、白细胞介素-1β(IL-1β)、白细胞介素-6(IL-6)的质量浓度。结果与正常对照组相比较,模型组左室收缩压(LVSP)和左室内压最大上升和下降速度(±dp/dtmax)降低,左室舒张末压(LVEDP)、心脏质量指数和左心室质量指数增高(P<0.05),血清TNF-α、IL-1β、IL-6水平增加(P<0.05)。与模型组相比较,PrG-L、PrG-M和PrG-H各组LVSP和±dp/dtmax升高,LVEDP、心脏质量指数和左心室质量指数下降(P<0.05),血清TNF-α、IL-1β、IL-6水平下降(P<0.05)。结论 PrG具有改善心肌纤维化的作用,其保护机制可能与下调TNF-α、IL-1β、IL-6水平有关。
Objective To investigate the effect of propyl gallate (PrG) on myocardial fibrosis induced by isoproterenol (Iso) in rats and its possible mechanism. Methods Fifty male Sprague-Dawley rats of 8 weeks old were randomly divided into normal control group, model group, low-dose of propyl gallate group (PrG-L group), middle-dose of propyl gallate group (PrG-M group) High-dose group (PrG-H group), 10 in each group. The back of the subcutaneous injection of Iso preparation MF model. After 7d, PrG-L, PrGM and PrG-H groups were given intraperitoneal injection of propyl gallate injection 18,36,72mg / kg, the normal control group and model group were injected with the same amount of saline as above. Regular observation of the state of rats, activities, diet, hair and other general conditions. After 4 weeks, the hemodynamic parameters of heart were measured and the indexes of cardiac mass index and left ventricular mass index were calculated. The levels of TNF-α, IL-1β ), Interleukin-6 (IL-6) mass concentration. Results Compared with the normal control group, LVSP and ± dp / dtmax, LVEDP, LVMI and left ventricular mass (P <0.05), and the levels of serum TNF-α, IL-1β and IL-6 increased (P <0.05). Compared with model group, LVSP and ± dp / dtmax increased, LVEDP, cardiac mass index and left ventricular mass index decreased (P <0.05) in PrG-L, PrG-M and PrG- IL-1β, IL-6 levels decreased (P <0.05). Conclusion PrG can improve myocardial fibrosis, and its protective mechanism may be related to down-regulating the levels of TNF-α, IL-1β and IL-6.