Luhong Formula Has a Cardioprotective Effect on Left Ventricular Remodeling in Pressure-Overloaded Rats
Luhong Formula Has a Cardioprotective Effect on Left Ventricular Remodeling in Pressure-Overloaded Rats
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鹿红方对压力超负荷大鼠左心室重构具有心脏保护作用
DOI：
10.1155/2020/4095967
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发表时间：
2020-05-30
影响因子：
--
通讯作者：
Lan, Zhen-Zhen
中科院分区：
文献类型：
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作者：
Liu, Qian;Qu, Hui-Yan;Lan, Zhen-Zhen
背景鹿红方-一种中药，含有鹿、红花，膜荚黄芪（Astragalus membranaceus（菲施.）BGE.变种蒙古黄芪[专业]植Hsiao，紫茎泽兰（French.）南夫，肉桂和独行菜被用于治疗心力衰竭，但对其作用机制知之甚少。我们研究了LHF的抗纤维化作用。方法.将48只SD雄性大鼠随机分为6组，每组8只，即模型组、假手术组、培哚普利组（0.036 mg/ml）、六味地黄丸高剂量组（LHF-H，1.44 g/mL）、中剂量组（LHF-M，0.72 g/mL）、低剂量组（LHF-L，0.36 g/mL）。除假手术组外，其余各组均行腹主动脉缩窄术建立心肌肥厚模型。测量HW和LVW以计算LVW/BW和HW/BW。ELISA法检测血清BNP浓度。Western blot检测心肌组织中eNOS、TGF-β 1、caspase-3、VEGF和VEGFR2的表达。RT-PCR检测心肌组织eNOS、Col1a1、Col3a1、TGF-β 1、VEGF、VEGFR2 mRNA表达。HE染色及天狼猩红染色，光镜下观察心肌组织形态及Ⅰ、Ⅲ型胶原纤维。结果与模型组相比，LHF治疗组的HW/BW、LVM/BW和BNP水平均显著降低。组织学和病理形态学观察表明，LHF可抑制心衰大鼠心肌纤维化。LHF处理上调心脏组织中eNOS的表达，下调Col1a1、Col3a1、TGF-β 1、caspase-3、VEGF和VEGFR2的表达。结论LHF可改善压力负荷性心力衰竭大鼠左室重构，其机制可能与心肌纤维化和细胞凋亡有关。eNOS表达上调和Col1a1、Col3a1、TGF-β 1、caspase-3、VEGF和VEGFR2表达下调可能在观察到的LHF心脏保护作用中发挥作用。
Background. Luhong formula (LHF)-a traditional Chinese medicine containing Cervus nippon Temminck, Carthamus tinctorius L., Astragalus membranaceus (Fisch.) Bge. var. mongholicus (Bge.) Hsiao, Codonopsis pilosula (Franch.) Nannf., Cinnamomum cassia Presl, and Lepidium apetalum Willd-is used in the treatment of heart failure, but little is known about its mechanism of action. We have investigated the effects of LHF on antifibrosis. Methods. Forty-eight SD male rats were randomly assigned into six groups (n = 8), model group, sham-operation group, perindopril group (0.036 mg/ml), LHF high doses (LHF-H, 1.44 g/mL), LHF middle doses (LHF-M, 0.72 g/mL), and LHF low doses (LHF-L, 0.36 g/mL). Except the sham-operation group, the other groups were received an abdominal aorta constriction to establish a model of myocardial hypertrophy. The HW and LVW were measured to calculate the LVW/BW and HW/BW. ELISA was used to detect the serum concentration of BNP. The expressions of eNOS, TGF-beta 1, caspase-3, VEGF, and VEGFR2 in heart tissues were assessed by western blot analysis. mRNA expressions of eNOS, Col1a1, Col3a1, TGF-beta 1, VEGF, and VEGFR2 in heart tissues were measured by RT-PCR. The specimens were stained with hematoxylin-eosin (HE) and picrosirius red staining for observing the morphological characteristics and collagen fibers I and III of the myocardium under a light microscope. Results. LHF significantly lowered the rat's HW/BW and LVM/BW, and the level of BNP in the LHF-treated group compared with the model group. Histopathological and pathomorphological changes of collagen fibers I and III showed that LHF inhibited myocardial fibrosis in heart failure rats. Treatment with LHF upregulated eNOS expression in heart tissue and downregulated Col1a1, Col3a1, TGF-beta 1, caspase-3, VEGF, and VEGFR2 expression. Conclusion. LHF can improve left ventricular remodeling in a pressure-overloaded heart failure rat model; this cardiac protective ability may be due to cardiac fibrosis and attenuated apoptosis. Upregulated eNOS expression and downregulated Col1a1, Col3a1, TGF-beta 1, caspase-3, VEGF, and VEGFR2 expression may play a role in the observed LHF cardioprotective effect.