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The protective effect of polyphyllin I on myocardial ischemia/reperfusion injury in rats

BACKGROUND: Myocardial ischemia/reperfusion (I/R) injury has become a global public health concern. An increasing amount of evidence has shown that polyphyllin I (PPI) has anti-apoptotic and antioxidant functions. This study was performed to evaluate the cardioprotective effects of PPI in a rat mode...

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Autores principales: Huang, Ruizhen, Shu, Jia, Dai, Xiaoqin, Liu, Yanru, Yu, Fang, Shi, Gang
Formato: Online Artículo Texto
Lenguaje:English
Publicado: AME Publishing Company 2020
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7290651/
https://www.ncbi.nlm.nih.gov/pubmed/32566581
http://dx.doi.org/10.21037/atm-20-3371
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author Huang, Ruizhen
Shu, Jia
Dai, Xiaoqin
Liu, Yanru
Yu, Fang
Shi, Gang
author_facet Huang, Ruizhen
Shu, Jia
Dai, Xiaoqin
Liu, Yanru
Yu, Fang
Shi, Gang
author_sort Huang, Ruizhen
collection PubMed
description BACKGROUND: Myocardial ischemia/reperfusion (I/R) injury has become a global public health concern. An increasing amount of evidence has shown that polyphyllin I (PPI) has anti-apoptotic and antioxidant functions. This study was performed to evaluate the cardioprotective effects of PPI in a rat model of myocardial I/R injury and the underlying mechanism. METHODS: We exposed induced a rat model of I/R injury by exposing rat hearts to left anterior descending coronary artery ligation for 30 min, followed by 24 h of reperfusion. Cardiac function was analyzed by echocardiography and HE staining. Myocardial apoptosis, inflammation, and oxidative stress were detected to analyze the PPI’s role in I/R injury. RESULTS: The results showed that pretreatment with PPI improved impaired histological morphology, as shown by histopathological examination. Echocardiography analysis showed that PPI increased the levels of HR, left ventricular ejection fraction (LVEF), and left ventricular wall thickness (LVWT), accompanied by decreased left ventricular end-systolic volume (LVESV). Also, PPI decreased the expression of CK-MB, Mb, cTnI, and LDH. Specifically, PPI also changed the expression of apoptotic makers (Caspase-3, Bax, and Bcl-2), inflammatory cytokines (TNF-α, IL-6, iNOS, and IL-10) and oxidative stress markers (SOD, GSH, ROS, and MDA). Notably, western blot (WB) showed that PPI treatment inhibited the phosphorylation activity of NF-κB p65. CONCLUSIONS: The findings showed that PPI exerted a favorable protective effect on I/R injury by inhibiting the inflammatory response and oxidative stress. It offered new drug candidates for the treatment of myocardial I/R injury.
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spelling pubmed-72906512020-06-19 The protective effect of polyphyllin I on myocardial ischemia/reperfusion injury in rats Huang, Ruizhen Shu, Jia Dai, Xiaoqin Liu, Yanru Yu, Fang Shi, Gang Ann Transl Med Original Article BACKGROUND: Myocardial ischemia/reperfusion (I/R) injury has become a global public health concern. An increasing amount of evidence has shown that polyphyllin I (PPI) has anti-apoptotic and antioxidant functions. This study was performed to evaluate the cardioprotective effects of PPI in a rat model of myocardial I/R injury and the underlying mechanism. METHODS: We exposed induced a rat model of I/R injury by exposing rat hearts to left anterior descending coronary artery ligation for 30 min, followed by 24 h of reperfusion. Cardiac function was analyzed by echocardiography and HE staining. Myocardial apoptosis, inflammation, and oxidative stress were detected to analyze the PPI’s role in I/R injury. RESULTS: The results showed that pretreatment with PPI improved impaired histological morphology, as shown by histopathological examination. Echocardiography analysis showed that PPI increased the levels of HR, left ventricular ejection fraction (LVEF), and left ventricular wall thickness (LVWT), accompanied by decreased left ventricular end-systolic volume (LVESV). Also, PPI decreased the expression of CK-MB, Mb, cTnI, and LDH. Specifically, PPI also changed the expression of apoptotic makers (Caspase-3, Bax, and Bcl-2), inflammatory cytokines (TNF-α, IL-6, iNOS, and IL-10) and oxidative stress markers (SOD, GSH, ROS, and MDA). Notably, western blot (WB) showed that PPI treatment inhibited the phosphorylation activity of NF-κB p65. CONCLUSIONS: The findings showed that PPI exerted a favorable protective effect on I/R injury by inhibiting the inflammatory response and oxidative stress. It offered new drug candidates for the treatment of myocardial I/R injury. AME Publishing Company 2020-05 /pmc/articles/PMC7290651/ /pubmed/32566581 http://dx.doi.org/10.21037/atm-20-3371 Text en 2020 Annals of Translational Medicine. All rights reserved. https://creativecommons.org/licenses/by-nc-nd/4.0/Open Access Statement: This is an Open Access article distributed in accordance with the Creative Commons Attribution-NonCommercial-NoDerivs 4.0 International License (CC BY-NC-ND 4.0), which permits the non-commercial replication and distribution of the article with the strict proviso that no changes or edits are made and the original work is properly cited (including links to both the formal publication through the relevant DOI and the license). See: https://creativecommons.org/licenses/by-nc-nd/4.0 (https://creativecommons.org/licenses/by-nc-nd/4.0/) .
spellingShingle Original Article
Huang, Ruizhen
Shu, Jia
Dai, Xiaoqin
Liu, Yanru
Yu, Fang
Shi, Gang
The protective effect of polyphyllin I on myocardial ischemia/reperfusion injury in rats
title The protective effect of polyphyllin I on myocardial ischemia/reperfusion injury in rats
title_full The protective effect of polyphyllin I on myocardial ischemia/reperfusion injury in rats
title_fullStr The protective effect of polyphyllin I on myocardial ischemia/reperfusion injury in rats
title_full_unstemmed The protective effect of polyphyllin I on myocardial ischemia/reperfusion injury in rats
title_short The protective effect of polyphyllin I on myocardial ischemia/reperfusion injury in rats
title_sort protective effect of polyphyllin i on myocardial ischemia/reperfusion injury in rats
topic Original Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7290651/
https://www.ncbi.nlm.nih.gov/pubmed/32566581
http://dx.doi.org/10.21037/atm-20-3371
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