Rutin protects against pirarubicin-induced cardiotoxicity by adjusting microRNA-125b-1-3p-mediated JunD signaling pathway

Li, Qi; Qin, Meng; Li, Tengteng; Gu, Zhengtao; Tan, Qi; Huang, Peng; Ren, Liqun

doi:10.1007/s11010-020-03696-9

Cited by 17 publications

(12 citation statements)

References 25 publications

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“…Moreover, in the same study, cardiomyocytes transfected with miR-125b-1-3p showed enhanced cell viability following simulated I/R injury. In contrast, Li and colleagues found that decreased level of miR-125b-1-3p is associated with rutin-induced cardioprotection in HL-1 cells [14]. These discrepancies may arise due to substantial differences in the applied models since the molecular mechanism of I/R may differ from the mechanisms of drug-induced cardiotoxicity.…”

Section: Discussionmentioning

confidence: 98%

Hypercholesterolemia Interferes with Induction of miR-125b-1-3p in Preconditioned Hearts

Szabó

Gáspár

Pipicz

et al. 2020

IJMS

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Ischemic preconditioning (IPre) reduces ischemia/reperfusion (I/R) injury in the heart. The non-coding microRNA miR-125b-1-3p has been demonstrated to play a role in the mechanism of IPre. Hypercholesterolemia is known to attenuate the cardioprotective effect of preconditioning; nevertheless, the exact underlying mechanisms are not clear. Here we investigated, whether hypercholesterolemia influences the induction of miR-125b-1-3p by IPre. Male Wistar rats were fed with a rodent chow supplemented with 2% cholesterol and 0.25% sodium-cholate hydrate for 8 weeks to induce high blood cholesterol levels. The hearts of normo- and hypercholesterolemic animals were then isolated and perfused according to Langendorff, and were subjected to 35 min global ischemia and 120 min reperfusion with or without IPre (3 × 5 min I/R cycles applied before index ischemia). IPre significantly reduced infarct size in the hearts of normocholesterolemic rats; however, IPre was ineffective in the hearts of hypercholesterolemic animals. Similarly, miR-125b-1-3p was upregulated by IPre in hearts of normocholesterolemic rats, while in the hearts of hypercholesterolemic animals IPre failed to increase miR-125b-1-3p significantly. Phosphorylation of cardiac Akt, ERK, and STAT3 was not significantly different in any of the groups at the end of reperfusion. Based on these results we propose here that hypercholesterolemia attenuates the upregulation of miR-125b-1-3p by IPre, which seems to be associated with the loss of cardioprotection.

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Section: Discussionmentioning

confidence: 98%

Hypercholesterolemia Interferes with Induction of miR-125b-1-3p in Preconditioned Hearts

Szabó

Gáspár

Pipicz

et al. 2020

IJMS

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“…In mouse myocardial ischemia-reperfusion model with highexpressed miR-125b, miR-125 protects the myocardium from ischemia/reperfusion (I/R) damage by inhibiting p53mediated apoptotic signals and NF-B activation mediated by TRAF 6, thus significantly reducing the myocardial infarction and preventing cardiac insufficiency (33). Li et al (34) transfected miR-125b-1-3p mimics into mouse cardiomyocytes, and the oxidative stress and apoptotic protein expressions were significantly increased. Other studies revealed that umbilical cord-derived MSCs significantly inhibit T lymphocyte proliferation by inducing T lymphocyte apoptosis and cell cycle arrest (14).…”

Section: Discussionmentioning

confidence: 99%

Human Adipose-derived mesenchymal stem cells promote lymphocyte apoptosis and alleviate atherosclerosis via miR-125b-1-3p/BCL11B signal axis

Tang

et al. 2021

Ann Palliat Med

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Background: Mesenchymal stem cells (MSCs) have shown great potential in the treatment of cardiovascular diseases, with fat being a more accessible source of MSCs. This study investigated the effect of human adipose-derived mesenchymal stem cells (hMSCs-Ad) exosomes on T lymphocytes and its role in atherosclerosis (AS).Methods: The exosomes were preliminarily isolated hMSCs-Ad and co-cultured with human H9 T lymphocytes. The effects of hMSCs-Ad exosomes on the proliferation and apoptosis of H9 were examined by performing functional experiments. The serum lipid level and inflammatory factor level in tail vein of mice were measured by biochemical analyzer and enzyme linked immunosorbent assay (ELISA) respectively. Results:The hMSCs-Ad-derived exosomes up-regulate the expression of micro (mi)R-125b-1-3p in H9 and AS arterial tissues. miR-125b-1-3p shared a targeted binding site with B-cell chronic lymphocytic leukemia (CLL)/lymphoma 11B gene (BCL11B). miR-125b-1-3p negatively regulated the expression of BCL11B in H9, and that knocking down BCL11B in H9 promoted its apoptosis. Injection of hMSCs-Adderived exosomes via the tail vein effectively reduced blood lipid and inflammatory factors, and that relieved the symptoms of AS in AS model mice.Conclusions: miR-125b-1-3p was expressed in hMSCs-Ad exosomes and can promote T lymphocyte apoptosis and alleviate AS by down-regulating BCL11B expression. It provides potential molecular targets for the clinical treatment of AS.

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“…The control group was injected with 1 mL of normal saline through the tail vein. The THP model group received tail vein injection of THP once a week [3 mg/kg each time (6)] for 6 consecutive weeks. The low-dose QSHWC (QSHWC-L) group received intragastric administration of QSHWC at 0.125 g/(kg•d) for 6 consecutive weeks in addition to 6 consecutive weeks of tail vein injection with THP (once a week, 3 mg/kg each time).…”

Section: Model Preparation and Grouping Interventionmentioning

confidence: 99%

Qishen Huanwu capsule reduces pirarubicin-induced cardiotoxicity in rats by activating the PI3K/Akt/mTOR pathway

Wang

Jiao

et al. 2020

Ann Palliat Med

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Background: One of the common adverse reactions to anthracyclines, a group of chemotherapeutics, is cardiotoxicity. Cancer patients receiving anthracycline-based chemotherapeutic regimens often discontinue treatment due to cardiotoxicity. How to prevent and reduce the cardiotoxicity of anthracyclines is one of the hot topics in the field of onco-cardiology. Traditional Chinese medicine can reduce the toxic side effects of chemotherapeutics. The present study aimed to investigate the protective effect of Qishen Huanwu capsule (QSHWC) on pirarubicin (THP)-induced myocardial injury in rats and the underlying mechanisms.Methods: Forty-eight male Sprague-Dawley (SD) rats were randomly divided into six groups: control group, THP, low-dose QSHWC, moderate-dose QSHWC, high-dose QSHWC, and LY294002[phosphatidylinositol 3-kinase (PI3K) inhibitor] (n=8 each). Echocardiographic examination was performed to examine heart structure and function. Hematoxylin and eosin (HE) staining was conducted to examine histopathological changes in myocardial tissue. Immunofluorescence staining was carried out to examine the expression of the autophagosome-specific marker protein microtubule-associated protein 1 light chain 3 (LC3). Western blot was performed to analyze the expression of LC3-I, LC3-II, PI3K, phosphorylated (p)-PI3K, protein kinase B (Akt), p-Akt, mammalian target of rapamycin (mTOR), and p-mTOR.Results: Compared with the control group, the THP group had a higher left ventricular end-systolic diameter (LVESD), lower left ventricular ejection fraction (LVEF), lower left ventricular fractional shortening (LVFS), and inferior heart function. In addition, compared with the control group, the THP group had significantly higher LC3 protein expression, a significantly higher LC3-II/LC3-I ratio (P<0.05), and significantly lower p-PI3K, p-Akt, and p-mTOR (P<0.05). QSHWC attenuated the THP-induced decline in heart function, downregulated LC3 protein in rat myocardial tissue, decreased the LC3-II/LC3-I ratio, and increased p-PI3K, p-Akt, and p-mTOR. In the LY294002 group, the above effects of QSHWC were reversed.Conclusions: QSHWC alleviated THP-induced myocardial injury. The underlying mechanism was related to the activation of the PI3K/Akt/mTOR pathway and the mitigation of the excessive autophagy of cardiomyocytes caused by THP.

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Rutin protects against pirarubicin-induced cardiotoxicity by adjusting microRNA-125b-1-3p-mediated JunD signaling pathway

Cited by 17 publications

References 25 publications

Hypercholesterolemia Interferes with Induction of miR-125b-1-3p in Preconditioned Hearts

Hypercholesterolemia Interferes with Induction of miR-125b-1-3p in Preconditioned Hearts

Human Adipose-derived mesenchymal stem cells promote lymphocyte apoptosis and alleviate atherosclerosis via miR-125b-1-3p/BCL11B signal axis

Qishen Huanwu capsule reduces pirarubicin-induced cardiotoxicity in rats by activating the PI3K/Akt/mTOR pathway

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