The protective role of lutein on isoproterenol-induced cardiac failure rat model through improving cardiac morphology, antioxidant status via positively regulating Nrf2/HO-1 signalling pathway

Ouyang, Bo; Li, Zili; Ji, Xiong-Ying; Huang, Jiang-Wei; Zhang, Hengsheng; Jiang, Chang-Rong

doi:10.1080/13880209.2019.1649436

Cited by 47 publications

(42 citation statements)

References 28 publications

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“…Similarly, the infarct size was also significantly increased in ISP‐induced rats owing to increased myocardial damage (necrosis and apoptosis) and results in a lack of oxygen (hypoxia) and glucose (mitochondrial dysfunction). Similar kind of results was also observed in other studies (Khan et al., 2019; Ouyang et al., 2019). The cardiac infarct size (area) was markedly reduced in TAN administered rats due to cardio preservative activity through abolishing mitochondrial dysfunction and enhance myocardial degeneration (Lu et al., 2018).…”

Section: Discussionsupporting

confidence: 91%

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A possible underlying mechanism behind the cardioprotective efficacy of tangeretin on isoproterenol triggered cardiotoxicity via modulating PI3K/Akt signaling pathway in a rat model

Zhang

Yang

et al. 2020

J Food Biochem

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This study was aimed to examine the possible underlying cardioprotective efficacy of tangeretin (TAN) in rats exposed to isoproterenol (ISP). Forty male SD rats were separated into four equal groups as the control group, ISP (myocardial infarction; MI group) group rats which were injected intraperitoneally (ip) with 85 mg/kg of ISP. Treatment TAN groups (TAN 50 and TAN 100) rats were orally pretreated with TAN (50 or 100 mg/kg) for 28 days before ISP exposure. Pretreatment with TAN (50/100) significantly reduced (p < .05/0.01) the infarct size, levels of inflammatory markers, cardiac marker enzymes, apoptotic markers along with improved antioxidants. Histo‐morphological results also well‐supported the results of the above biochemical parameters by displaying normal myofibrillar arrangement in TAN pretreated rats. Moreover, the protein expressions of pPI3K and pAkt were considerably elevated in rats administered with TAN. Collectively, TAN pretreatment (especially TAN 100) display better cardioprotective activity against ISP‐induced MI rats. Practical applications Tangeretin (TAN) has been reported to exhibit an array of biological functions including cardioprotective, hepatoprotective, and renoprotective activities. However, the in‐depth mechanism is still lacking, which results in this study. Our results indicate that TAN could effectively reduce cardiac infarct size, inflammatory markers, oxidative stress, apoptotic markers, by modulating (upregulating) the protein expressions of the PI3K/Akt signaling pathway. Thus, demonstrating that TAN could be a strong contender for developing a cardioprotective agent and can recommend along with conventional cardioprotective drugs for abolishing MI‐related complications/symptoms. Nevertheless, further human studies are needed to confirm the above suggestion.

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Section: Discussionsupporting

confidence: 91%

“…Even though currently we have many treatment regimens to minimize the risk of MI and its related symptomatic condition but till date no effective remedies are available. Hence, many researchers are still working to find an effective cardioprotective agent that can lower the risk of MI (Heusch & Gersh, 2017; Ouyang et al., 2019).…”

Section: Introductionmentioning

confidence: 99%

A possible underlying mechanism behind the cardioprotective efficacy of tangeretin on isoproterenol triggered cardiotoxicity via modulating PI3K/Akt signaling pathway in a rat model

Zhang

Yang

et al. 2020

J Food Biochem

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“…The biochemical and histopathological changes of lutein (40 mg/kg, p.o., for 28 days) against isoproterenol (ISO)-induced (85 mg/kg, s.c., for two consecutive days) myocardial infarction (MI) rat model was evaluated by Ouyang et al 38 . Their results suggested that pretreatment with lutein "significantly reduced infarction size, lipid peroxidation product, cardiac markers [(lactate dehydrogenase (LDH), creatine kinase-MB (CK-MB) and cardiac troponin T (cTn T)], inflammatory markers (IL-1β, IL-6, TNF-α and NF-κB p65), and apoptotic markers (caspase-3 and -9)".…”

Section: Cardioprotective Activitymentioning

confidence: 99%

“…Their results suggested that pretreatment with lutein "significantly reduced infarction size, lipid peroxidation product, cardiac markers [(lactate dehydrogenase (LDH), creatine kinase-MB (CK-MB) and cardiac troponin T (cTn T)], inflammatory markers (IL-1β, IL-6, TNF-α and NF-κB p65), and apoptotic markers (caspase-3 and -9)". 38 In addition, lutein significantly increased antioxidant levels [catalase (CAT) and SOD] as well as dramatically upregulated HO-1 and Nrf-2 protein expressions. In addition, lutein significantly reversed all the histopathological changes and thus confirmed its cardioprotection.…”

Section: Cardioprotective Activitymentioning

confidence: 99%

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Lutein: A Comprehensive Review on its Chemical, Biological Activities and Therapeutic Potentials

Fuad¹,

Sekar²,

Gan³

et al. 2020

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To complete this review, relevant literatures were collected from several scientific databases, include Google Scholar, Pubmed and ScienceDirect between 2000 to till date. The categories of keywords used were "Lutein" and "Sources" or "Pharmacological Studies" or "Molecular Mechanism" or "Biological Properties" or "Chemistry" or "Food Industry" or "Food Products" or "Formulations" or "Health Benefits". Studies which are not written in English and have no abstracts have been excluded from initial screening. There was no restriction to be followed for collecting the lutein-related studies, particularly in animal and human studies. After applying the inclusion and exclusion criteria and removing duplicates from the ABSTRACT Background: Lutein is a naturally occurring carotenoid found in high amounts in flowers, grains, fruits and green vegetables with green leaves include spinach, kale and carrots. The market for lutein encompasses pharmaceutical, dietary supplement, food, animal and fish feed industries. Objective: The present review aimed to provide an updated and comprehensive analysis of lutein, including its chemistry, biological properties and therapeutic potentials. Methods: Relevant literatures were collected from several scientific databases, include Google Scholar, Pubmed and ScienceDirect between 2000 to till date. Following a detailed inclusion and exclusion screening process, the information obtained was summarized. Results: Information on the sources, chemistry and biological properties including antioxidant, anti-arthrisits, antiinflammatory, hepatoprotective, cardioprotective, anti-cataract, antidiabetic, anticancer and bone remodelling activities, as well as food industry processing for lutein were tabled. Lutein can be considered powerful antioxidants along with multifaceted molecular targets, such as NF-ҡB, PI3K/Akt, Nrf-2, HO-1 and SIRT-1 signaling pathways in various pathological conditions. Conclusion: The present review observe the chemical, pharmacological properties, in addition to the therapeutic potentials of lutein. It is hoped that the information can provide a good reference to aid in the development and utilization of lutein in phytopharmaceuticals and food industries.

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Lutein exerts its cardioprotective effect against the experimental model of isoprenaline‐induced myocardial infarction via MIAT/miR‐200a/Nrf2/TXINP pathway

Abdelmonem

Ibrahim

Essam

et al. 2021

J Biochem & Molecular Tox

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Acute myocardial infarction (AMI) remains a leading cause of morbidity and mortality worldwide. Lutein (LU) possesses numerous pharmacological activities, including anti‐inflammatory, antioxidant, and antiapoptotic effects. This study aimed to investigate the cardioprotective potential of LU in isoprenaline (ISO)‐induced MI and to explore its molecular mechanisms of action. AMI was induced by two consecutive subcutaneous doses of ISO (65 mg/kg; s.c.). The LU group was pretreated with LU (20 mg/kg; p.o.) for 30 days followed by ISO injections on Days 29 and 30. ISO group showed elevated serum creatine kinas‐MB (CK‐MB) and considerable electrocardiographic changes along with reduced ejection fraction compared to the normal group. LU pretreatment could decrease serum CK‐MB activity, normalize QRS and QTc intervals and restore ejection fraction compared to the untreated group. The ISO group demonstrated infarcted‐like lesions, which were ameliorated in the LU‐pretreated group. Immunohistochemical investigation revealed upregulated cardiac troponin T (cTn T) and desmin expressions in the LU‐pretreated group. LU pretreatment also enhanced cardiac thioredoxin (Trx) and glutathione (GSH) contents as well as reduced lipid peroxidation, compared to the untreated group. Importantly, LU pretreatment could downregulate long noncoding MI associated transcript (lncRNA MIAT) and thioredoxin‐interacting protein (TXNIP) and augment micro RNA (miR)‐200a and nuclear factor erythroid 2‐related factor 2 (Nrf2) expressions compared to the ISO group. Moreover, a significant inverse correlation between MIAT and miR‐200a was observed. In conclusion, this study revealed that LU could ameliorate ISO‐induced MI in rats by modulating MIAT/miR‐200a/Nrf2 pathway.

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The protective role of lutein on isoproterenol-induced cardiac failure rat model through improving cardiac morphology, antioxidant status via positively regulating Nrf2/HO-1 signalling pathway

Cited by 47 publications

References 28 publications

A possible underlying mechanism behind the cardioprotective efficacy of tangeretin on isoproterenol triggered cardiotoxicity via modulating PI3K/Akt signaling pathway in a rat model

A possible underlying mechanism behind the cardioprotective efficacy of tangeretin on isoproterenol triggered cardiotoxicity via modulating PI3K/Akt signaling pathway in a rat model

Lutein: A Comprehensive Review on its Chemical, Biological Activities and Therapeutic Potentials

Lutein exerts its cardioprotective effect against the experimental model of isoprenaline‐induced myocardial infarction via MIAT/miR‐200a/Nrf2/TXINP pathway

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