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Quercetin Ameliorates Myocardial Injury in Diabetic Rats by Regulating Autophagy and Apoptosis through AMPK/mTOR Signaling Pathway.

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Title: Quercetin Ameliorates Myocardial Injury in Diabetic Rats by Regulating Autophagy and Apoptosis through AMPK/mTOR Signaling Pathway.
Authors: Chen, Yong-Feng (AUTHOR), Qiu, Qi (AUTHOR), Wang, Lei (AUTHOR), Li, Xiao-Rong (AUTHOR), Zhou, Shun (AUTHOR), Wang, Heng (AUTHOR), Jiang, Wen-Di (AUTHOR), Geng, Jia-Yi (AUTHOR), Qin-Gao (AUTHOR), Tang, Bi (AUTHOR), Wang, Hong-Ju (AUTHOR), Kang, Pin-Fang (AUTHOR)
Source: American Journal of Chinese Medicine. 2024, Vol. 52 Issue 3, p841-864. 24p.
Subjects: Myocardial infarction, Proteins, In vitro studies, Flow cytometry, Autophagy, Research funding, Apoptosis, Cellular signal transduction, In vivo studies, Descriptive statistics, Fluorescent antibody technique, Quercetin, Rats, Gene expression, Cell culture, Animal experimentation, Western immunoblotting, One-way analysis of variance, Stains & staining (Microscopy), Data analysis software, Diabetes, Echocardiography
Abstract: A high-glucose environment is involved in the progression of diabetes mellitus (DM). This study aims to explore the regulatory effects of quercetin (QUE) on autophagy and apoptosis after myocardial injury in rats with DM. The type 2 DM rat models were constructed using low-dose streptozotocin (STZ) treatment combined with a high-carbohydrate (HC) diet in vivo. Compared with the control group, the body weight was decreased, whereas blood pressure, blood glucose, and the LVW/BW ratio were increased in the diabetic group. The results showed that the myocardial fibers were disordered in the diabetic group. Moreover, we found that the myocardial collagen fibers, PAS-positive cells, and apoptosis were increased, whereas the mitochondrial structure was destroyed and autophagic vacuoles were significantly reduced in the diabetic group compared with the control group. The expression levels of autophagy-related proteins LC3 and Beclin1 were decreased, whereas the expression levels of P62, Caspae-3, and Bax/Bcl-2 were increased in the diabetic group in vitro and in vivo. Moreover, QUE treatment alleviated the cellular oxidative stress reaction under high-glucose environments. The results of immunoprecipitation (IP) showed that the autophagy protein Beclin1 was bound to Bcl-2, and the binding capacity increased in the HG group, whereas it decreased after QUE treatment, suggesting that QUE inhibited the binding capacity between Beclin1 and Bcl-2, thus leading to the preservation of Beclin1-induced autophagy. In addition, the blood pressure, blood glucose, and cardiac function of rats were improved following QUE treatment. In conclusion, QUE suppressed diabetic myocardial injury and ameliorated cardiac function by regulating myocardial autophagy and inhibition of apoptosis in diabetes through the AMPK/mTOR signaling pathway. [ABSTRACT FROM AUTHOR]
Copyright of American Journal of Chinese Medicine is the property of World Scientific Publishing Company and its content may not be copied or emailed to multiple sites without the copyright holder's express written permission. Additionally, content may not be used with any artificial intelligence tools or machine learning technologies. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)
Database: Psychology and Behavioral Sciences Collection
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An: 177537794
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Items – Name: Title
  Label: Title
  Group: Ti
  Data: Quercetin Ameliorates Myocardial Injury in Diabetic Rats by Regulating Autophagy and Apoptosis through AMPK/mTOR Signaling Pathway.
– Name: Author
  Label: Authors
  Group: Au
  Data: <searchLink fieldCode="AR" term="%22Chen%2C+Yong-Feng%22">Chen, Yong-Feng</searchLink> (AUTHOR)<br /><searchLink fieldCode="AR" term="%22Qiu%2C+Qi%22">Qiu, Qi</searchLink> (AUTHOR)<br /><searchLink fieldCode="AR" term="%22Wang%2C+Lei%22">Wang, Lei</searchLink> (AUTHOR)<br /><searchLink fieldCode="AR" term="%22Li%2C+Xiao-Rong%22">Li, Xiao-Rong</searchLink> (AUTHOR)<br /><searchLink fieldCode="AR" term="%22Zhou%2C+Shun%22">Zhou, Shun</searchLink> (AUTHOR)<br /><searchLink fieldCode="AR" term="%22Wang%2C+Heng%22">Wang, Heng</searchLink> (AUTHOR)<br /><searchLink fieldCode="AR" term="%22Jiang%2C+Wen-Di%22">Jiang, Wen-Di</searchLink> (AUTHOR)<br /><searchLink fieldCode="AR" term="%22Geng%2C+Jia-Yi%22">Geng, Jia-Yi</searchLink> (AUTHOR)<br /><searchLink fieldCode="AR" term="%22Qin-Gao%22">Qin-Gao</searchLink> (AUTHOR)<br /><searchLink fieldCode="AR" term="%22Tang%2C+Bi%22">Tang, Bi</searchLink> (AUTHOR)<br /><searchLink fieldCode="AR" term="%22Wang%2C+Hong-Ju%22">Wang, Hong-Ju</searchLink> (AUTHOR)<br /><searchLink fieldCode="AR" term="%22Kang%2C+Pin-Fang%22">Kang, Pin-Fang</searchLink> (AUTHOR)
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  Data: <searchLink fieldCode="JN" term="%22American+Journal+of+Chinese+Medicine%22">American Journal of Chinese Medicine</searchLink>. 2024, Vol. 52 Issue 3, p841-864. 24p.
– Name: Subject
  Label: Subjects
  Group: Su
  Data: <searchLink fieldCode="DE" term="%22Myocardial+infarction%22">Myocardial infarction</searchLink><br /><searchLink fieldCode="DE" term="%22Proteins%22">Proteins</searchLink><br /><searchLink fieldCode="DE" term="%22In+vitro+studies%22">In vitro studies</searchLink><br /><searchLink fieldCode="DE" term="%22Flow+cytometry%22">Flow cytometry</searchLink><br /><searchLink fieldCode="DE" term="%22Autophagy%22">Autophagy</searchLink><br /><searchLink fieldCode="DE" term="%22Research+funding%22">Research funding</searchLink><br /><searchLink fieldCode="DE" term="%22Apoptosis%22">Apoptosis</searchLink><br /><searchLink fieldCode="DE" term="%22Cellular+signal+transduction%22">Cellular signal transduction</searchLink><br /><searchLink fieldCode="DE" term="%22In+vivo+studies%22">In vivo studies</searchLink><br /><searchLink fieldCode="DE" term="%22Descriptive+statistics%22">Descriptive statistics</searchLink><br /><searchLink fieldCode="DE" term="%22Fluorescent+antibody+technique%22">Fluorescent antibody technique</searchLink><br /><searchLink fieldCode="DE" term="%22Quercetin%22">Quercetin</searchLink><br /><searchLink fieldCode="DE" term="%22Rats%22">Rats</searchLink><br /><searchLink fieldCode="DE" term="%22Gene+expression%22">Gene expression</searchLink><br /><searchLink fieldCode="DE" term="%22Cell+culture%22">Cell culture</searchLink><br /><searchLink fieldCode="DE" term="%22Animal+experimentation%22">Animal experimentation</searchLink><br /><searchLink fieldCode="DE" term="%22Western+immunoblotting%22">Western immunoblotting</searchLink><br /><searchLink fieldCode="DE" term="%22One-way+analysis+of+variance%22">One-way analysis of variance</searchLink><br /><searchLink fieldCode="DE" term="%22Stains+%26+staining+%28Microscopy%29%22">Stains & staining (Microscopy)</searchLink><br /><searchLink fieldCode="DE" term="%22Data+analysis+software%22">Data analysis software</searchLink><br /><searchLink fieldCode="DE" term="%22Diabetes%22">Diabetes</searchLink><br /><searchLink fieldCode="DE" term="%22Echocardiography%22">Echocardiography</searchLink>
– Name: Abstract
  Label: Abstract
  Group: Ab
  Data: A high-glucose environment is involved in the progression of diabetes mellitus (DM). This study aims to explore the regulatory effects of quercetin (QUE) on autophagy and apoptosis after myocardial injury in rats with DM. The type 2 DM rat models were constructed using low-dose streptozotocin (STZ) treatment combined with a high-carbohydrate (HC) diet in vivo. Compared with the control group, the body weight was decreased, whereas blood pressure, blood glucose, and the LVW/BW ratio were increased in the diabetic group. The results showed that the myocardial fibers were disordered in the diabetic group. Moreover, we found that the myocardial collagen fibers, PAS-positive cells, and apoptosis were increased, whereas the mitochondrial structure was destroyed and autophagic vacuoles were significantly reduced in the diabetic group compared with the control group. The expression levels of autophagy-related proteins LC3 and Beclin1 were decreased, whereas the expression levels of P62, Caspae-3, and Bax/Bcl-2 were increased in the diabetic group in vitro and in vivo. Moreover, QUE treatment alleviated the cellular oxidative stress reaction under high-glucose environments. The results of immunoprecipitation (IP) showed that the autophagy protein Beclin1 was bound to Bcl-2, and the binding capacity increased in the HG group, whereas it decreased after QUE treatment, suggesting that QUE inhibited the binding capacity between Beclin1 and Bcl-2, thus leading to the preservation of Beclin1-induced autophagy. In addition, the blood pressure, blood glucose, and cardiac function of rats were improved following QUE treatment. In conclusion, QUE suppressed diabetic myocardial injury and ameliorated cardiac function by regulating myocardial autophagy and inhibition of apoptosis in diabetes through the AMPK/mTOR signaling pathway. [ABSTRACT FROM AUTHOR]
– Name: AbstractSuppliedCopyright
  Label:
  Group: Ab
  Data: <i>Copyright of American Journal of Chinese Medicine is the property of World Scientific Publishing Company and its content may not be copied or emailed to multiple sites without the copyright holder's express written permission. Additionally, content may not be used with any artificial intelligence tools or machine learning technologies. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract.</i> (Copyright applies to all Abstracts.)
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RecordInfo BibRecord:
  BibEntity:
    Identifiers:
      – Type: doi
        Value: 10.1142/S0192415X24500344
    Languages:
      – Code: eng
        Text: English
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        PageCount: 24
        StartPage: 841
    Subjects:
      – SubjectFull: Myocardial infarction
        Type: general
      – SubjectFull: Proteins
        Type: general
      – SubjectFull: In vitro studies
        Type: general
      – SubjectFull: Flow cytometry
        Type: general
      – SubjectFull: Autophagy
        Type: general
      – SubjectFull: Research funding
        Type: general
      – SubjectFull: Apoptosis
        Type: general
      – SubjectFull: Cellular signal transduction
        Type: general
      – SubjectFull: In vivo studies
        Type: general
      – SubjectFull: Descriptive statistics
        Type: general
      – SubjectFull: Fluorescent antibody technique
        Type: general
      – SubjectFull: Quercetin
        Type: general
      – SubjectFull: Rats
        Type: general
      – SubjectFull: Gene expression
        Type: general
      – SubjectFull: Cell culture
        Type: general
      – SubjectFull: Animal experimentation
        Type: general
      – SubjectFull: Western immunoblotting
        Type: general
      – SubjectFull: One-way analysis of variance
        Type: general
      – SubjectFull: Stains & staining (Microscopy)
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      – SubjectFull: Data analysis software
        Type: general
      – SubjectFull: Diabetes
        Type: general
      – SubjectFull: Echocardiography
        Type: general
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      – TitleFull: Quercetin Ameliorates Myocardial Injury in Diabetic Rats by Regulating Autophagy and Apoptosis through AMPK/mTOR Signaling Pathway.
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              Text: 2024
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