Effect of Traditional Chinese Medicine Poge Heart-Saving Decoction on Cardiac Function in Heart Failure Rat Model.
Effect of Traditional Chinese Medicine Poge Heart-Saving Decoction on Cardiac Function in Heart Failure Rat Model.
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DOI：
10.1155/2020/8762509
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发表时间：
2020
期刊：
影响因子：
--
通讯作者：
Sun B
中科院分区：
文献类型：
--
作者：
Liu L;Mo Y;Wu B;Yu Z;Sun B
破葛救心汤在我国作为治疗心力衰竭的药物已有多年的历史。本研究旨在探讨PHSD对心力衰竭患者心功能的影响及其机制。 采用阿霉素（Adriamycin）诱导大鼠心力衰竭（HF）模型。将60只大鼠随机分为6组：空白对照组、假手术组、9.33 g/kg剂量组（低剂量组）、13.995 g/kg剂量组（中剂量组）、18.66 g/kg剂量组（高剂量组）和福辛普利组（4.67 mg/kg，对照组）。采用心脏超声评价大鼠心功能，放射免疫法测定血清醛固酮（ALD）和血管紧张素II（AngII）水平。 与空白对照组比较，假手术组左室舒张末期内径（LVEDd）和左室收缩末期内径（LVEDs）均增大（1.04 ± 0.12 vs.0.67 ± 0.13 cm; 0.75 ± 0.13 vs.0.28 ± 0.10 cm; P < 0.05），左室射血分数降低（36.65 ± 5.74vs.76.09 ± 4.23%; P < 0.05）。9.33 g/kg组、13.995 g/kg组和18.66 g/kg组大鼠的射血分数较假手术组增加（57.13 ± 1.63、58.43 ± 1.98和59.21 ± 1.37 vs.36.65 ± 5.74%; P < 0.05）。PHSD还通过降低LVEDd和LVEDs改善心功能（0.88 ± 0.11、0.75 ± 0.13和0.72 ± 0.18 vs. 1.04 ± 0.12 cm; 0.62 ± 0.10、0.63 ± 0.17和0.45 ± 0.11 vs. 0.75 ± 0.13 cm; P < 0.05）。假手术组大鼠血清中ALD和AngII水平明显高于空白对照组（371.58 ± 39.25 vs. 237.12 ± 17.35 μg/L; 232.18 ± 16.33 vs. 159.44 ± 18.42 pg/L; P < 0.05）。PHSD各组及福辛普利组ALD、AngII均降低（276.81 ± 25.63、277.18 ± 21.35、268.19 ± 19.28、271.47 ± 28.96）μg/L对371.58 ± 39.25 μg/L; 169.41 ± 27.53、168.81 ± 19.78、164.23 ± 21.34和174.27 ± 22.84对232.18 ± 16.33 pg/L; P < 0.05）。假手术组心肌组织病理学改变为纤维排列紊乱、染色模糊、断裂、带状。除假手术组和空白对照组外，其余各组大鼠心肌断裂均减轻。 因此，PHSD可缩短大鼠LVEDd和LVEDs，逆转心室重构。其机制可能与抑制肾素-血管紧张素-醛固酮系统（尤其是ALD和AngII）的激活水平，降低心脏后负荷有关。
Poge heart-saving decoction (PHSD) has been used as a medicine treating heart failure in China for many years. The study aimed to explore the effect of PHSD on cardiac function in heart failure conditions and its underlying mechanism. Adriamycin was used to induce the model of heart failure (HF) in rats. Sixty rats were randomly divided into six groups: blank control group, sham group, 9.33 g/kg group (low-PHSD, test group), 13.995 g/kg group (moderate-PHSD, test group), 18.66 g/kg group (high-PHSD, test group), and fosinopril group (4.67 mg/kg, comparison test group). Cardiac ultrasound was used to evaluate the cardiac function of the rats, and radioimmunoassay was used to measure aldosterone (ALD) and angiotensin II (AngII) levels in the serum. Compared with the blank control group, the left ventricular end-diastolic dimension (LVEDd) and left ventricular end-systolic dimension (LVEDs) in the sham group were increased (1.04 ± 0.12 vs. 0.67 ± 0.13 cm; 0.75 ± 0.13 vs. 0.28 ± 0.10 cm; P < 0.05), and the left ventricular ejection fraction was decreased (36.65 ± 5.74 vs. 76.09 ± 4.23%; P < 0.05). The ejection fraction of HF rats was increased in 9.33 g/kg group, 13.995 g/kg group, and 18.66 g/kg group compared with those of the sham group (57.13 ± 1.63, 58.43 ± 1.98, and 59.21 ± 1.37 vs. 36.65 ± 5.74%; P < 0.05). PHSD also improved cardiac function by reducing the LVEDd and LVEDs (0.88 ± 0.11, 0.75 ± 0.13, and 0.72 ± 0.18 vs. 1.04 ± 0.12 cm; 0.62 ± 0.10, 0.63 ± 0.17, and 0.45 ± 0.11 vs. 0.75 ± 0.13 cm; P < 0.05). The levels of ALD and AngII in the serum of rats in the sham group were significantly higher than those in the blank control group (371.58 ± 39.25 vs. 237.12 ± 17.35 μg/L; 232.18 ± 16.33 vs. 159.44 ± 18.42 pg/L; P < 0.05). The ALD and AngII of the rats in all of the three PHSD groups and the fosinopril group were decreased (276.81 ± 25.63, 277.18 ± 21.35, 268.19 ± 19.28, and 271.47 ± 28.96 vs. 371.58 ± 39.25 μg/L; 169.41 ± 27.53, 168.81 ± 19.78, 164.23 ± 21.34, and 174.27 ± 22.84 vs. 232.18 ± 16.33 pg/L; P < 0.05). The histopathological changes of the myocardium in the sham group showed the disorganized fiber, shaded staining, fracture, and zonation. The fracture of the myocardium was relieved in all groups except the sham group and the blank control group. Therefore, PHSD could shorten LVEDd and LVEDs of rats and reverse ventricular remodeling. The mechanism might be related to the inhibition of the activation level of renin-angiotensin-aldosterone system (especially ALD and AngII) and decreasing the postload of the heart.
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