Anti-depressive effect of Shuangxinfang on rats with acute myocardial infarction: Promoting bone marrow mesenchymal stem cells mobilization and alleviating inflammatory response

Wang, Chao; Hou, Jiqiu; Du, Hongsen; Yan, Shasha; Yang, Jingjing; Wang, Yun; Zhang, Xiujing; Zhu, Lili; Zhao, Haibin

doi:10.1016/j.biopha.2018.11.113

Cited by 9 publications

(8 citation statements)

References 43 publications

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“…There are some laboratory achievements for the molecule compounds of components in PCF consistent with the in ammatory mechanism obtained in our study. Our previous research suggested that PCF reduced the in ammatory reaction derived from myocardial ischemia, and changed the expression of neurotransmitters directly by modifying the expression of GAD67 to relieve depression [17]. The published literature showed that the tanshinone IIA and salvianolate, as bioactive chemical constitutes from the root of Salvia miltiorrhiza, have signi cant advantage in cardiovascular protective effects, as well as the e cacy of anti-in ammatory and myocardial protective [63].…”

Section: Discussionmentioning

confidence: 99%

“…Furthermore, the pharmacological mechanism of PCF is concentrated on regulation of in ammatory response and neuroendocrinology system. PCF could inhibit the expression of in ammatory factors such as tumor necrosis factor-α (TNF-α) in AMI rats, and meanwhile appease the neural system by modulating the γ-aminobutyric acid (GABA) system [17]. The above data highlighted a critical role for the PCF in inhibiting in ammation caused by injured myocardium and alleviating depression following AMI.…”

Section: Introductionmentioning

confidence: 92%

“…PCF was purchased from Beijing Pharmaceutical Co. Ltd. One dosage of PCF composed of: Salvia miltiorrhiza 20 g, Rhizoma chuanxiong 12 g, Semen ziziphi spinosae 30 g and lily bulb 30 g. One dosage of PCF was dissolved in 100 ml distilled water. The optimal lavage dose was 1ml/100g/d according to preliminary tests [17]. Paquinimod (Apexbio, Houston, USA), also called ABR-215757 (a speci c inhibitor of S100A9), binds to S100A9 in a Ca 2+ /Zn 2+ dependent way and blocks interaction with TLR4 [23,24].…”

Section: Drugs and Reagentsmentioning

confidence: 99%

“…As described previously, ligation of the left anterior descending (LAD) coronary artery was used to construct AMI rat model, while only threading was operated without knotting in the sham group [17,30].…”

Section: Establishment Of Ami Rat Modelmentioning

confidence: 99%

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Shuangxinfang prevents S100A9-induced macrophage/microglial inflammation to improve cardiac function and depression-like behaviour in rats after acute myocardial infarction

Sun¹,

Wang

Hou³

et al. 2021

Preprint

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Background Depression is a common complication of cardiovascular disease, which deteriorated the cardiac function. Shuangxinfang (Psycho-cardiology Formula, PCF) was reported to alleviate myocardial ischemia injury and improve depression-like behavior. Interestingly, our previous proteomics study predicted that the protein S100A9 appeared as an important target, and macrophage/microglial inflammation might be involved in the process of PCF treating depressive disorder induced by acute myocardial infarction (AMI). The aim of this study is to validate the proteomics results. Methods AMI rat models were established in vivo, followed by the administration of PCF or ABR-215757 (also named paquinimod, inhibiting S100A9 binding to TLR4) for 5 days. Forced swimming test (FST) and open field test (OFT) were applied to record depression-like behavior, and echocardiography was employed to evaluate cardiac function. Morphological changes of cardiomyocytes were assessed by HE staining and TUNEL staining on day 7 after cardiac surgery, as well as masson trichrome staining on day 21. Hippocampal neurogenesis was determined by Nissl staining, while 5-hydroxytryptamine (5-HT) and brain-derived neurotrophic factor (BDNF) in the hippocampus were detected as biochemical indicators of depression. Myocardial and hippocampal expression of inflammatory factors were analyzed by western blotting, immunofluorescence, and ELISA. The activation state of macrophage and microglia was assessed via immunoreaction respectively using CD68 and Iba1. For in vitro confirmation, BV2 cells were primed with recombinant protein S100A9, and then pretreated with PCF serum, to determine alterations in microglial activation and inflammation. Results Rats in the AMI group showed heart function deterioration, as well as depression-like behavior. Coronary ligation not only brought about myocardial inflammation, cell apoptosis and fibrosis, but also reduced the neurogenesis and decreased the content of 5-HT. PCF could ameliorate the pathological and phenotypic changes of the heart and brain, and inhibited the expression of S100A9/TLR4/NF-κB pathway, the activation of microglial cell and the secretion of IL-1β and TNF-α raised by AMI. ABR-215757 showed therapeutic effect and molecular biological mechanisms similar to PCF. Pretreatment with PCF serum in vitro was proved to efficiently block the hyperactivation of BV2 cells and increasement of cytokine contents induced by recombinant protein S100A9. Conclusion We identify S100A9 as a novel and potent regulator of inflammation in both heart and brain. Macrophage/microglia inflammation mediated by S100A9 is considered as a pivotal pathogenic in depression post-AMI, as well as a major pathway for the treatment of PCF, suggesting that PCF is a promising therapeutic candidate for psycho-cardiology disease.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 92%

Section: Drugs and Reagentsmentioning

confidence: 99%

Section: Establishment Of Ami Rat Modelmentioning

confidence: 99%

See 2 more Smart Citations

Shuangxinfang prevents S100A9-induced macrophage/microglial inflammation to improve cardiac function and depression-like behaviour in rats after acute myocardial infarction

Sun¹,

Wang

Hou³

et al. 2021

Preprint

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“…exhibited a cardio-protective effect (9)(10)(11). However, the exact mechanisms involved in cHd in combination with depression are still mostly unknown and effective medicines are limited.…”

Section: Kai-xin-san Suppresses Matrix Metalloproteinases and Myocardmentioning

confidence: 99%

Kai‑Xin‑San suppresses matrix metalloproteinases and myocardial apoptosis in rats with myocardial infarction and depression

Dong

Zhang

et al. 2019

Mol Med Report

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depression is often triggered by prolonged exposure to psychosocial stressors and associated with coronary heart disease (cHd). Matrix metalloproteinases (MMPs) are involved in the pathogenesis of various emotional and cardiovascular disorders. The purpose of this study was to investigate whether Kai-Xin-San (KXS), which may terminate the signaling of MMPs, exerts antidepressant-like and cardioprotective effects in a myocardial infarction (Mi) plus depression rat model. Rats were randomly assigned to five groups: a normal control (control group), a celisc-injection of isopropyl adrenaline group (iSo group), depression (depression group), an iSo + depression (depression + iSo group), and an iSo + depression group treated with intragastric administration of 1,785 mg/kg KXS (KXS group). Behavioral changes, echocardiography, biochemical index, matrix metalloproteinase (MMP) and apoptosis-related proteins were assessed. compared with the depression + iSo group, KXS significantly improved stress-induced alterations of behavioral parameters and protected the heart by enlarging the left ventricular (lV) fractional shortening (FS) and lV ejection fraction (EF). Moreover, KXS significantly attenuated iSo + depression-induced MMP-2 and MMP-9 expression at the mrna and protein level and decreased TiMP in the heart compared to the complex model group. Myocardial apoptosis was significantly attenuated by KXS by regulating the Bcl-2/Bax axis. These results indicated that Mi comorbid with depression may damage the MMP balance in the central and peripheral system, and KXS may have a direct anti-depressive and cardio-protective effect by regulating the level of MMPs and associated myocardial apoptosis. it is promising to further explore the clinical potential of KXS for the therapy or prevention of Mi plus depression comorbidity disease.

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Mesenchymal Stem Cell-Derived Extracellular Vesicle-Shuttled microRNA-302d-3p Represses Inflammation and Cardiac Remodeling Following Acute Myocardial Infarction

Liu

Guan

Yan

et al. 2022

J. of Cardiovasc. Trans. Res.

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Anti-depressive effect of Shuangxinfang on rats with acute myocardial infarction: Promoting bone marrow mesenchymal stem cells mobilization and alleviating inflammatory response

Cited by 9 publications

References 43 publications

Shuangxinfang prevents S100A9-induced macrophage/microglial inflammation to improve cardiac function and depression-like behaviour in rats after acute myocardial infarction

Shuangxinfang prevents S100A9-induced macrophage/microglial inflammation to improve cardiac function and depression-like behaviour in rats after acute myocardial infarction

Kai‑Xin‑San suppresses matrix metalloproteinases and myocardial apoptosis in rats with myocardial infarction and depression

Mesenchymal Stem Cell-Derived Extracellular Vesicle-Shuttled microRNA-302d-3p Represses Inflammation and Cardiac Remodeling Following Acute Myocardial Infarction

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