Myricetin against myocardial injury in rat heat stroke model

Lin, Xin; Lin, Chih‐Ming; Liu, Ruoxu; Li, Chenyi; Jiao, Shuxin; Yi, Xueqing; Walker, Michael J.; Xu, Xiao Ming; Zhao, Tengda; Huang, Po-Chang

doi:10.1016/j.biopha.2020.110194

Cited by 15 publications

(12 citation statements)

References 34 publications

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“…However, myricetin treatment ameliorated MDA significantly and dose dependently, possibly by scavenging ROS as reported previously . Very recently, Lin et al (2020) have reported that myricetin significantly decreases MDA levels in cardiopathic rats by upregulating HSP-72 . Myricetin has well been reported to substantially inhibit ROS generation with simultaneous activation of anti-oxidative enzymes in H 2 O 2 -induced cell damage …”

Section: Discussionsupporting

confidence: 62%

“…59 Very recently, Lin et al (2020) have reported that myricetin significantly decreases MDA levels in cardiopathic rats by upregulating HSP-72. 60 Myricetin has well been reported to substantially inhibit ROS generation with simultaneous activation of antioxidative enzymes in H 2 O 2 -induced cell damage. 61 Various enzymatic and non-enzymatic antioxidants remove free radicals in biological systems, acting as an effective defense against ROS.…”

Section: Discussionmentioning

confidence: 99%

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Myricetin (3,3′,4′,5,5′,7-Hexahydroxyflavone) Prevents 5-Fluorouracil-Induced Cardiotoxicity

et al. 2022

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5-Fluorouracil (5-FU) is a strong anti-cancer drug used to manage numerous cancers. Cardiotoxicity, renal toxicity, and liver toxicity are some of the adverse effects which confine its clinical use to some extent. 5-FU-induced organ injuries are associated with redox imbalance, inflammation, and damage to heart functioning, particularly in the present study. Myricetin is an abundant flavonoid, commonly extracted from berries and herbs having anti-oxidative and anti-cancer activities. We planned the current work to explore the beneficial effects of myricetin against 5-FU-induced cardiac injury in Wistar rats through a biochemical and histological approach. Prophylactic myricetin treatment at two doses (25 and 50 mg/kg) was given to rats orally for 21 days against cardiac injury induced by a single injection of 5-FU (150 mg/kg b.wt.) given on the 20th day intraperitoneally. The 5-FU injection induced oxidative stress, inflammation, and extensive cardiac damage. Nevertheless, myricetin alleviated markers of inflammation, apoptosis, cardiac toxicity, oxidative stress, and upregulated anti-oxidative machinery. The histology of heart further supports our biochemical findings mitigated by the prophylactic treatment of myricetin. Henceforth, myricetin mitigates 5-FU-induced cardiac damage by modulating oxidative stress, inflammation, and cardiacspecific markers, as found in the present study.

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Section: Discussionsupporting

confidence: 62%

Section: Discussionmentioning

confidence: 99%

Myricetin (3,3′,4′,5,5′,7-Hexahydroxyflavone) Prevents 5-Fluorouracil-Induced Cardiotoxicity

et al. 2022

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“…Moreover, the mechanism of RFS-related myocardial injury remains to be elucidated. It has been reported that CK-MB, LDH, and cTnI are markers of myocyte injury (34), and myocardial apoptosis is also a prognostic indicator of myocardial injury (35). Appearance of a reduction in cardiac contractility following a diffuse multifocal inflammatory infiltrate, myocardial fiber disorganization, cardiomyocyte apoptosis, and increased expression of CK-MB, LDH, and cTnI in our study indicated the occurrence of severe myocardial injury induced by SCR.…”

Section: Discussionsupporting

confidence: 60%

SIRT3-mediated mitochondrial autophagy in refeeding syndrome-related myocardial injury in sepsis rats

Li¹,

Lu²,

Zhang³

et al. 2022

Ann Transl Med

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Background: Myocardial injury induced by refeeding syndrome (RFS) is one of the important causes of deterioration in critically ill patients. Sirtuin-3 (SIRT3) has been shown to regulate mitochondrial autophagy in myocardial ischemia/reperfusion injury; however, the role of mitochondrial autophagy on RFS-related myocardial injury in patients in critical condition has not been reported on.Methods: Thirty Sprague-Dawley (SD) rats were divided into 3 groups (n=10 each group): the control group; the standard calorie refeeding (SCR) group; and the low calorie refeeding (LCR) group. The rats were weighed every third or four days from day 1 to day 14. On day 14, all rats were anesthetized and received an echocardiography test. Blood and bronchoalveolar lavage fluid (BALF) were collected and tested for arterial oxygen pressure (PaO 2 ), phosphorus (P), and calcium (Ca), creatine kinase-MB (CK-MB), lactate dehydrogenase (LDH), and cardiac troponin 1 (cTnI), myeloperoxidase (MPO), tumor necrosis factor α (TNF-α), interleukin-1β (IL-1β), and IL-6. The histopathological change of hearts and lungs were evaluated, and lung injury score was calculated. Mitochondrial autophagy related proteins (including Beclin1, LC3, mitofusin-2, Mfn2, PINK1, Parkin, and SIRT3) were analyzed using a Western blot. To evaluate the effect of SIRT3, 20 rats were divided into 2 groups (n=10 each group): The adeno-associated virus 9 (AAV9-Nc) group; and the AAV9-SIRT3 overexpression (AAV9-SIRT3) group. The protocols for rats were the same as the SCR group since day 22 after injection of AAV9. The protein expressions of PINK1, Parkin, and SIRT3 were compared between the AAV9-Nc group and AAV9-SIRT3 group.Results: SCR caused significant decline in cardiac contractility and increased inflammatory cell infiltration in myocardial tissue. Meanwhile, Beclin1, LC3, PINK1, Parkin, and SIRT3 levels decreased, while Mfn2 showed no significant change. Furthermore, significant positive correlations were also found between SIRT3 and P, PINK1, and Parkin, and significant negative correlations were found between SIRT3 and CK-MB, LDH, and cTnI. Overexpression of SIRT3 activated the PINK1/Parkin mediated mitochondrial autophagy.Conclusions: SIRT3 has an essential role in RFS-related myocardial injury during LPS induced chronic sepsis in rats, probably via regulating mitochondrial autophagy.

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“…The administration of myricetin after heart injury rescued pyrimidine biosynthesis in nonmyocyte cells, augmented cardiac repair, and postinfarct heart function [ 20 ]. Since some other flavonoid compounds were also reported to elicit anti-myocardial ischemic effects [ 21 , 22 , 23 , 24 , 25 , 26 , 27 , 28 , 29 ], some other mechanisms including antioxidant and anti-inflammatory activities might also be involved with myricetin [ 30 , 31 , 32 ]. Novel flavonoid ENPP1 inhibitors might have similar therapeutic potential to rescue cardiac injury and thus are greatly needed.…”

Section: Introductionmentioning

confidence: 99%

From Myricetin to the Discovery of Novel Natural Human ENPP1 Inhibitors: A Virtual Screening, Molecular Docking, Molecular Dynamics Simulation, and MM/GBSA Study

Song

Shao

2022

Molecules

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It was recently revealed that naturally occurring myricetin can inhibit ectonucleotidase ectonucleotide pyrophosphatase/phosphodiesterase 1 (ENPP1), which, in turn, can treat ischemic cardiac injury. However, due to myricetin’s poor druggability, its further developments are relatively limited, which necessitates the discovery of novel ENPP1-inhibiting myricetin analogs as alternatives. In this study, the binding model of myricetin with ENPP1 was elucidated by molecular docking and molecular dynamics studies. Subsequently, virtual screening on the self-developed flavonoid natural product database (FNPD), led to the identification of two flavonoid glycosides (Cas No: 1397173-50-0 and 1169835-58-8), as potential ENPP1 inhibitors. Docking scores and MM/GBSA binding energies predicted that they might have higher inhibitory effects than myricetin. This study provides a strong foundation for the future development of ischemic cardiac injury drugs.

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Myricetin against myocardial injury in rat heat stroke model

Cited by 15 publications

References 34 publications

Myricetin (3,3′,4′,5,5′,7-Hexahydroxyflavone) Prevents 5-Fluorouracil-Induced Cardiotoxicity

Myricetin (3,3′,4′,5,5′,7-Hexahydroxyflavone) Prevents 5-Fluorouracil-Induced Cardiotoxicity

SIRT3-mediated mitochondrial autophagy in refeeding syndrome-related myocardial injury in sepsis rats

From Myricetin to the Discovery of Novel Natural Human ENPP1 Inhibitors: A Virtual Screening, Molecular Docking, Molecular Dynamics Simulation, and MM/GBSA Study

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