| 徐基杰,戴健,李晓惠,等.鹿红方抗心肌纤维化作用及对STAT3的影响[J].浙江中医药大学学报,2024,48(9):1074-1082. |
| 鹿红方抗心肌纤维化作用及对STAT3的影响 |
| Effects of Luhong Formula on Myocardial Fibrosis and STAT3 |
| DOI：10.16466/j.issn1005-5509.2024.09.003 |
| 中文关键词: 慢性心力衰竭 心肌梗死 鹿红方 心肌纤维化 信号转导及转录激活因子3 促纤维化因子 心肾阳虚 心肾同治 |
| 英文关键词: chronic heart failure myocardial infarction Luhong Formula myocardial fibrosis signal transduction and transcriptional activator 3 pro-fibrotic factor heart-kidney Yang deficiency heart-kidney synergy therapy |
| 基金项目:上海市科学技术委员会医学创新研究专项面上项目(21Y11920100)；国家自然科学基金项目(81904016) |
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| 中文摘要: |
| [目的] 研究鹿红方改善心肌梗死后心肌纤维化的作用机制。[方法] 采用冠状动脉结扎法制备心肌梗死后心肌纤维化模型。将60只SD大鼠随机分配至假手术组、模型组、鹿红方组以及培哚普利组，干预4周后用心脏彩色多普勒超声检查测量心脏结构和左室射血分数，苏木精-伊红(hematoxylin-eosin，HE)染色、Masson和天狼星红染色观察心脏组织纤维化病理改变，免疫印迹检测心脏信号转导及转录激活因子3(signal transducer and activator of transcription 3，STAT3)分泌情况，酶联免疫吸附分析(enzyme-linked immunosorbent assay，ELISA)检测血清促纤维化因子结缔组织生长因子(connective tissue growth factor，CTGF)、血小板反应蛋白-1(thrombospondin-1，TSP-1)、基质金属蛋白酶抑制剂-1(tissue inhibitor of metalloproteinase-1，TIMP-1)的水平。[结果] 心脏彩色多普勒超声检查提示，与模型组比较，鹿红方和培哚普利干预均可抑制左室舒张末容积和左室舒张末内径的增大，而且使左室射血分数明显提升(P<0.05)。与培哚普利组比较，鹿红方组改善心室不良扩大与提高左室射血分数作用相近。HE染色结果显示，与模型组比较，鹿红方组和培哚普利组异常形态的心肌细胞数目明显减少，细胞间质肿胀减轻，炎症细胞浸润减少。Masson和天狼星红染色结果显示，与模型组比较，鹿红方组和培哚普利组干预均可减轻心肌纤维化病变程度。鹿红方组改善上述心肌病理改变和减轻心肌纤维化作用与培哚普利组相近。免疫印迹检测显示，与模型组比较，鹿红方和培哚普利干预均可增加心肌STAT3分泌(P<0.05)，鹿红方组促进心肌分泌STAT3的作用与培哚普利组相近，差异无统计学意义(P>0.05)。ELISA结果显示，与模型组比较，鹿红方组与培哚普利组CTGF、TSP-1、TIMP-1水平显著降低(P<0.05)，鹿红方组抑制CTGF、TSP-1和TIMP-1分泌作用与培哚普利组相近，差异无统计学意义(P>0.05)。[结论] 鹿红方可显著抑制心肌梗死后心肌纤维化，其机制与上调STAT3水平，抑制促纤维化因子CTGF、TSP-1和TIMP-1分泌有关。 |
| 英文摘要: |
| [Objective] To study the mechanism of Luhong Formula in relieving myocardial fibrosis after myocardial infarction. [Methods] The myocardial fibrosis model after myocardial infarction was prepared by coronary artery ligation. Sixty SD rats were randomly assigned to sham operation group， model group， Luhong Formula group and Perindopril group. Each group completed the corresponding intervention for 4 weeks. Heart structure and left ventricular ejection fraction were measured by ultrasonic cardiogram. The pathological changes of cardiac fibrosis were observed by hematoxylin-eosin(HE) staining， Masson and Sirius red staining. The secretion of cardiac signal transduction and activator of transcription 3(STAT3) was analyzed by Western blot. Enzyme-linked immunosorbent assay(ELISA) was used to detect the serum levels of pro-fibrotic factor including connective tissue growth factor(CTGF)， platelet reactive protein-1(TSP-1) and matrix metalloproteinase inhibitor-1(TIMP-1). [Results] Compared with model group， the intervention of Luhong Formula and Perindopril could inhibit the increase of left ventricular enddiastolic volume and left ventricular enddiastolic diameter， while the value of left ventricular ejection fraction was significantly increased (P<0.05). The effect of Luhong Formula group on improving ventricular dysdilation and increasing left ventricular ejection fraction was similar to that of Perindopril group. HE staining results showed that compared with model group， the number of abnormal cardiomyocytes in Luhong Formula group and Perindopril group was significantly reduced， the interstitial swelling was reduced， and the inflammatory cell infiltration was reduced. Masson and Sirius red staining showed that compared with model group， both Luhong Formula group and Perindopril group could reduce the degree of myocardial fibrosis after intervention. The effect of Luhong Formula group on improving the myocardial pathological changes and alleviating myocardial fibrosis was similar to that of Perindopril group. Western blot results showed that compared with model group， intervention in both Luhong Formula group and Perindopril group could significantly increase the myocardial STAT3 secretion(P<0.05)， and the effect of Luhong Formula group on promoting myocardial STAT3 secretion was similar to that of Perindopril group(P>0.05). ELISA results showed that the levels of CTGF， TSP-1 and TIMP-1 in Luhong Formula group and Perindopril group were significantly lower than those in model group(P<0.05)， and the inhibitory effects of CTGF， TSP-1 and TIMP-1 in Luhong Formula group were similar to those in Perindopril group(P>0.05). [Conclusion] Luhong Formula can significantly inhibit myocardial fibrosis after myocardial infarction， and its mechanism is related to up-regulating STAT3 level and inhibiting the secretion of pro-fibrotic factors CTGF， TSP-1 and TIMP-1. |
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