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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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DOI   10.11656/j.issn.1673-9043.2026.07.11
Key Words   pulmonary heart disease;Yishen Huashi Granule;autophagy;inflammatory cytokines;fibrosis;CIRBP-OGFR pathway
Author NameAffiliation
SHI Shuxia Department of Medical Education, Shijiazhuang Eighth Hospital, Shijiazhuang 050081, China 
GUO Wenhao Second Department of Cardiovascular Medicine, Hengshui Fourth People's Hospital, Hengshui 053000, China 
WANG Yan Third Department of Psychiatry, Shijiazhuang Eighth Hospital, Shijiazhuang 050081, China 
PAN Junwei Department of Neurology, Lincheng County People's Hospital, Xingtai 054399, China 
ZHANG Huanfang Department of Neurology, Lincheng County People's Hospital, Xingtai 054399, China 
QIAO Defeng Department of Traditional Chinese Medicine, Shijiazhuang Eighth Hospital, Shijiazhuang 050081, China 
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.

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