Protective effects of luteolin-7-O-glucoside against starvation-induced injury through upregulation of autophagy in H9c2 Cells

Yao, Hong; Zhou, Lichun; Tang, Linlin; Guan, Yanhui; Shang, Chao; Han, Xiuzhen

doi:10.5582/bst.2017.01111

Cited by 16 publications

(7 citation statements)

References 31 publications

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“…Despite some controversial findings exist, the role of AKT/mTOR pathway in MI remains debatable . Possible explanations may be addressed on the excessive or injured autophagy happens during disease progression. According to our results, we observed that autophagy is negatively associated with PI3K/AKT/mTOR/p70S6K signaling in a rat MI model, which is consistent with some studies focused on the cardioprotective role of autophagy [43][44][45]. Therefore, we declared that Iva activated the injured autophagy via inhibiting PI3K/AKT/ mTOR/p70S6K signaling in this study.…”

Section: Discussionsupporting

confidence: 91%

Ivabradine protects rats against myocardial infarction through reinforcing autophagy via inhibiting PI3K/AKT/mTOR/p70S6K pathway

et al. 2021

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Ivabradine (Iva), a heart rate reducing agent that specifically inhibits the pacemaker I(f) ionic current, has been demonstrated to be cardioprotective in many cardiovascular diseases. Autophagy is an evolutionarily conserved metabolic process that regulates cardiac homeostasis. This study is aimed to explore whether autophagy is functionally involved in the cardioprotective effect of Iva in a rat model of myocardial infarction (MI). We observed that Iva treatment (po, 10 mg/kg/day) showed significant recovery on the hemodynamics parameters in MI rats, including left ventricular systolic pressure, left ventricular end diastolic pressure, and maximal ascending/ descending rate of left ventricular pressure. Also, Iva treatment dramatically decreased infarct size, inhibited myocardial apoptosis, and reduced the levels of pro-inflammatory cytokines tumor necrosis factor (TNF)-α, interleukin (IL)-1β and IL-6 in MI rats. Moreover, Iva treatment enhanced autophagy and inhibited PI3K/AKT/mTOR/p70S6K pathway in MI rats. Simultaneously, we observed that autophagy enhancer rapamycin (ip, 10 mg/kg/day) showed similar cardioprotective effects with Iva. Furthermore, we observed that addition of autophagy inhibitor 3-methyladenine (ip, 10 mg/kg/day) counteracted the therapeutic effect of Iva, addressing that Iva attenuated post-MI cardiac injury by enhancing autophagy. In summary, these findings demonstrated that Iva attenuated MI in rats by enhancing autophagy, and PI3K/AKT/mTOR/p70S6K pathway might be involved in the process. Autophagy activation by Iva may be a potential therapeutic strategy for the treatment of MI.

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Section: Discussionsupporting

confidence: 91%

Ivabradine protects rats against myocardial infarction through reinforcing autophagy via inhibiting PI3K/AKT/mTOR/p70S6K pathway

et al. 2021

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“…Luteolin did not exhibit any notable effect itself at these concentrations. Thus, 10 µM was chosen as the concentration for luteolin for the rest of our study, consistent with previous reports (Yao et al, 2016(Yao et al, , 2017Bustos et al, 2018;Park et al, 2018;Zhou et al, 2018b). Neither doxorubicin nor luteolin (at various concentrations), or both, overtly affected resting cell length, TPS and TR 90 (P > 0.05).…”

Section: Luteolin Improved Cardiomyocyte Shortening and Relengtheningsupporting

confidence: 67%

Luteolin Attenuates Doxorubicin-Induced Cardiotoxicity Through Promoting Mitochondrial Autophagy

Sun

et al. 2020

Front. Physiol.

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Doxorubicin is a valuable antineoplastic drug although its clinical use is greatly hindered by its severe cardiotoxicity with dismal target therapy available. Luteolin is a natural product extracted from vegetables and fruits with a wide range of biological efficacies including anti-oxidative, anti-tumorigenic, and anti-inflammatory properties. This study was designed to examine the possible effect of luteolin on doxorubicin-induced cardiotoxicity, if any, and the mechanism(s) involved with a focus on mitochondrial autophagy. Luteolin application (10 µM) in adult mouse cardiomyocytes overtly improved doxorubicin-induced cardiomyocyte contractile dysfunction including elevated peak shortening amplitude and maximal velocity of shortening/relengthening along with unchanged duration of shortening and relengthening. Luteolin alleviated doxorubicininduced cardiotoxicity including apoptosis, accumulation of reactive oxygen species (ROS) and loss of mitochondrial membrane potential. Furthermore, luteolin attenuated doxorubicin-induced cardiotoxicity through promoting mitochondrial autophagy in association with facilitating phosphorylation of Drp1 at Ser 616 , and upregulating TFEB expression. In addition, luteolin treatment partially attenuated low dose doxorubicininduced elongation of mitochondria. Treatment of Mdivi-1, a Drp1 GTPase inhibitor, negated the protective effect of luteolin on levels of TFEB, LAMP1, and LC3B, as well as loss of mitochondrial membrane potential and cardiomyocyte contractile dysfunction in the face of doxorubicin challenge. Taken together, these findings provide novel insights for the therapeutic efficacy of luteolin against doxorubicin-induced cardiotoxicity possibly through improved mitochondrial autophagy.

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“…Thin-layer chromatography was performed on 0.20 mm Silica Gel 60 F254 plates (Qingdao Haiyang Chemical, China). 1 H NMR and 13 C NMR spectra were recorded on a Bruker Avance 400 spectrometer (Bruker Company, Germany) or a Varian spectrometer (Varian, Palo Alto, CA, USA), using tetramethylsilane as an internal standard. Chemical shifts were given in parts per million.…”

Section: Chemistrymentioning

confidence: 99%

Novel HDAC6 selective inhibitors with 4-aminopiperidine-1- carboxamide as the core structure enhanced growth inhibitory activity of bortezomib in MCF-7 cells

Zhao

Gao

Zhang

et al. 2019

BST

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In epigenetics, histone deacetylases (HDACs) are well validated targets for the development of anticancer drugs. In this work, we reported the design and synthesis of a series of twentytwo novel (E)-N-hydroxycinnamamide-based HDAC inhibitors with 4-aminopiperidine-1-carboxamide as the core structure. Most newly synthesized compounds displayed high inhibition rates toward HDAC at the concentration of 1 μM. Among them, the inhibition rates of compounds LYP-2, LYP-3, LYP-6, and LYP-15 were more than 75%. Furthermore, compounds LYP-2, LYP-3, and LYP-6 potently inhibited the activity of HDAC6 with selectivity over HDAC1. We chose LYP-2 and LYP-6 to test its antiproliferative effect on breast cancer cells MCF-7. Either LYP-2 or LYP-6 alone moderately suppressed the cell growth, but could synergistically enhance the inhibitory effect of bortezomib. These results suggested that combined HDAC6 inhibitor and bortezomib regimen might be an option for breast cancer treatment.

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Protective effects of luteolin-7-O-glucoside against starvation-induced injury through upregulation of autophagy in H9c2 Cells

Cited by 16 publications

References 31 publications

Ivabradine protects rats against myocardial infarction through reinforcing autophagy via inhibiting PI3K/AKT/mTOR/p70S6K pathway

Ivabradine protects rats against myocardial infarction through reinforcing autophagy via inhibiting PI3K/AKT/mTOR/p70S6K pathway

Luteolin Attenuates Doxorubicin-Induced Cardiotoxicity Through Promoting Mitochondrial Autophagy

Novel HDAC6 selective inhibitors with 4-aminopiperidine-1- carboxamide as the core structure enhanced growth inhibitory activity of bortezomib in MCF-7 cells

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