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| 益肾化湿颗粒改善肺源性心脏病心肌纤维化机制研究 |
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石书霞1, 郭文昊2, 王艳3, 潘俊伟4, 张焕芳4, 乔德峰5
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1.石家庄市第八医院医教科, 石家庄 050081;2.衡水市第四人民医院心血管内二科, 衡水 053000;3.石家庄市第八医院精神三科, 石家庄 050081;4.临城县人民医院神经内科, 邢台 054399;5.石家庄市第八医院中医科, 石家庄 050081
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| 摘要: |
| [目的] 探究益肾化湿颗粒对肺源性心脏病（简称肺心病）大鼠心肌纤维化的影响及机制。[方法] 建立肺心病模型大鼠，分为模型组、益肾化湿颗粒低（3.125 g/kg）、高（6.250 g/kg）剂量组，另取正常大鼠作为对照，每组10只。药物干预4周后，检测大鼠右心功能及动脉血气；酶联免疫吸附（ELISA）法检测大鼠血清白细胞介素-1β（IL-1β）、白细胞介素-6（IL-6）和肿瘤坏死因子-α（TNF-α）水平；苏木精-伊红（HE）和Masson染色观察心肌损伤情况；免疫组织化学染色观察心肌组织血小板内皮细胞黏附分子31（CD31）和α-平滑肌肌动蛋白（α-SMA）表达水平；透射电镜观察心肌细胞自噬情况；蛋白免疫印迹（Western blot）法检测心肌组织微管相关蛋白1轻链3 Ⅱ/Ⅰ（LC3 Ⅱ/Ⅰ）、Beclin-1、冷诱导RNA结合蛋白（CIRBP）及阿片生长因子受体（OGFR）蛋白表达水平。[结果] 与对照组比较，模型组大鼠呼吸频率、呼气峰流速值（PEF）、50%肺活量时最大呼气流量（FEF50）、动脉氧分压（PaO2）、氧饱和度（SaO2）降低，呼气阻力、动脉二氧化碳分压（PaCO2）、右心指数升高（P<0.05）；血清中IL-1β、IL-6、TNF-α水平升高（P<0.05）；心肌组织病理损伤严重，胶原纤维沉积率、α-SMA阳性率、OGFR蛋白表达水平升高，CD31阳性率、LC3 Ⅱ/Ⅰ、Beclin-1及CIRBP蛋白表达水平降低（P<0.05）。与模型组比较，益肾化湿颗粒低、高剂量组大鼠呼吸频率、PEF、FEF50、PaO2、SaO2升高，呼气阻力、PaCO2、右心指数降低（P<0.05）；血清中IL-1β、IL-6、TNF-α水平降低（P<0.05）；心肌组织病理损伤减轻，胶原纤维沉积率、α-SMA阳性率、OGFR蛋白表达水平降低，CD31阳性率、LC3 Ⅱ/Ⅰ、Beclin-1及CIRBP蛋白表达水平升高（P<0.05），且益肾化湿颗粒治疗效果呈剂量相关性（P<0.05）。[结论] 益肾化湿颗粒可以抑制肺心病大鼠炎症反应及心肌纤维化，其作用机制可能与激活心肌细胞自噬、调控CIRBP-OGFR通路相关。 |
| 关键词: 肺源性心脏病 益肾化湿颗粒 自噬 炎症因子 纤维化 CIRBP-OGFR通路 |
| DOI：10.11656/j.issn.1673-9043.2026.07.11 |
| 分类号:R285.5 |
| 基金项目:河北省中医药类科学研究课题计划项目（2022195）。 |
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| A study on the ameliorative effect and mechanisms of Yishen Huashi Granules on myocardial fibrosis in pulmonary heart disease |
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SHI Shuxia1, GUO Wenhao2, WANG Yan3, PAN Junwei4, ZHANG Huanfang4, QIAO Defeng5
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1.Department of Medical Education, Shijiazhuang Eighth Hospital, Shijiazhuang 050081, China;2.Second Department of Cardiovascular Medicine, Hengshui Fourth People's Hospital, Hengshui 053000, China;3.Third Department of Psychiatry, Shijiazhuang Eighth Hospital, Shijiazhuang 050081, China;4.Department of Neurology, Lincheng County People's Hospital, Xingtai 054399, China;5.Department of Traditional Chinese Medicine, Shijiazhuang Eighth Hospital, Shijiazhuang 050081, China
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| Abstract: |
| [Objective] To investigate the effect and mechanism of Yishen Huashi Granules（YSHS）on myocardial fibrosis in rats with pulmonary heart disease（PHD）. [Methods] A rat model of PHD was established and divided into model group，YSHS low（3.125 g/kg）-and high-dose（6.250 g/kg）groups；normal rats served as control （n=10 per group）. After 4-week drug intervention，right-heart function and arterial blood gases were measured；serum IL-1β， IL-6 and TNF-α levels were determined by ELISA；myocardial injury was evaluated by HE and Masson staining； CD31 and α-SMA expression was detected by immunohistochemistry；cardiomyocyte autophagy was observed by transmission electron microscopy；and protein levels of LC3-Ⅱ/Ⅰ，Beclin-1，CIRBP and OGFR in myocardium were quantified by Western blot. [Results] Compared with control，PHD model rats exhibited decreased respiratory rate，PEF，FEF50，PaO2 and SaO2，increased expiratory resistance，PaCO2 and right-heart index（P<0.05），elevated serum IL-1β，IL-6 and TNF-α（P<0.05），severe myocardial pathological damage，higher collagen deposition rate， α-SMA positivity and OGFR expression，and lower CD31 positivity，LC3-Ⅱ/Ⅰ ratio，Beclin-1 and CIRBP levels（P<0.05）. Relative to model group，YSHS low-and high-dose groups showed reversed changes in respiratory and hemodynamic parameters，reduced serum inflammatory cytokines，attenuated myocardial injury，decreased collagen deposition，α-SMA and OGFR expression，and increased CD31 positivity，LC3-Ⅱ/Ⅰ ratio，Beclin-1 and CIRBP levels（P<0.05），with dose-dependent efficacy（P<0.05）. [Conclusion] YSHS can suppress inflammation and myocardial fibrosis in PHD rats，presumably by activating cardiomyocyte autophagy and modulating the CIRBP-OGFR pathway. |
| Key words: pulmonary heart disease Yishen Huashi Granule autophagy inflammatory cytokines fibrosis CIRBP-OGFR pathway |
