The cardioprotective effects of acteoside in myocardial ischemia reperfusion injury and the underlying mechanism
Abstract Introduction We observed the cardioprotective effects of Acteoside (AC) on myocardial ischemia reperfusion injury (MIRI) and discussed the possible mechanisms. Methods Before MIRI model was established successfully, AC was administrated to SD rats by gastric route for 7 d. Punctuate paw wit...
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BMC
2025-04-01
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| Series: | BMC Cardiovascular Disorders |
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| Online Access: | https://doi.org/10.1186/s12872-025-04762-0 |
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| author | Jing Li Yuxin Guo Yang Yang Qing Xue Hong Cao Guangyuan Yang Zhiqi Sun Lin-Lin Jia Hai-Bo Yu |
| author_facet | Jing Li Yuxin Guo Yang Yang Qing Xue Hong Cao Guangyuan Yang Zhiqi Sun Lin-Lin Jia Hai-Bo Yu |
| author_sort | Jing Li |
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| description | Abstract Introduction We observed the cardioprotective effects of Acteoside (AC) on myocardial ischemia reperfusion injury (MIRI) and discussed the possible mechanisms. Methods Before MIRI model was established successfully, AC was administrated to SD rats by gastric route for 7 d. Punctuate paw withdrawal threshold (PWT) was recorded to reflect the pain threshold. Blood samples were collected to measure the levels of oxidative stress, myocardial enzymes and Norepinephrine (NE). Hematoxylin and eosin (HE) staining was performed to observe the pathological changes of myocardial tissues. Apoptosis of myocardial cell was determined by transferase-mediated dUTP nick end labeling (TUNEL) assay, and the expressions of Bcl-2 and Bax were determined by Western blotting. Using network pharmacological analysis, the PI3K/Akt signaling pathway was screened to be associated with both AC and MIRI. Subsequently, the expressions of PI3K, p-Akt and caspase-3 were detected by immunochemistry in myocardial tissues. Results We found that pre-administration of AC improved pain threshold and pathological change of myocardial structure caused by MIRI. AC reduced serum levels of myocardial enzymes and NE in MIRI. Compared with the Sham group, rats in MIRI group showed enhanced oxidative stress levels. These changes were partly reversed by AC. In addition, AC inhibited apoptosis, regulated the expression of apoptosis-related proteins. Immunochemistry analysis confirmed that AC increased the expressions of PI3K and p-Akt in myocardial tissue. Conclusion The cardioprotective effects of AC in MIRI were related with pain alleviation, oxidative stress, apoptosis and sympathetic nerve activity inhibition, the PI3K/Akt signal pathway activation. Clinical trial number Not applicable. |
| format | Article |
| id | doaj-art-52a0fc924ebc45b09a02b96a475b4f52 |
| institution | OA Journals |
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| language | English |
| publishDate | 2025-04-01 |
| publisher | BMC |
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| series | BMC Cardiovascular Disorders |
| spelling | doaj-art-52a0fc924ebc45b09a02b96a475b4f522025-08-20T02:30:19ZengBMCBMC Cardiovascular Disorders1471-22612025-04-0125111210.1186/s12872-025-04762-0The cardioprotective effects of acteoside in myocardial ischemia reperfusion injury and the underlying mechanismJing Li0Yuxin Guo1Yang Yang2Qing Xue3Hong Cao4Guangyuan Yang5Zhiqi Sun6Lin-Lin Jia7Hai-Bo Yu8Department of Physiology, Basic medical college, Jiamusi UniversityDepartment of Physiology, Basic medical college, Jiamusi UniversityDepartment of Physiology, Basic medical college, Jiamusi UniversityDepartment of Cardiology, the First affiliated hospital to Jiamusi UniversityDepartment of Cardiology, the First affiliated hospital to Jiamusi UniversityDepartment of Cardiology, the First affiliated hospital to Jiamusi UniversityDaqing Oilfield General HospitalDepartment of Physiology, Basic medical college, Jiamusi UniversityDepartment of Cardiology, the First affiliated hospital to Jiamusi UniversityAbstract Introduction We observed the cardioprotective effects of Acteoside (AC) on myocardial ischemia reperfusion injury (MIRI) and discussed the possible mechanisms. Methods Before MIRI model was established successfully, AC was administrated to SD rats by gastric route for 7 d. Punctuate paw withdrawal threshold (PWT) was recorded to reflect the pain threshold. Blood samples were collected to measure the levels of oxidative stress, myocardial enzymes and Norepinephrine (NE). Hematoxylin and eosin (HE) staining was performed to observe the pathological changes of myocardial tissues. Apoptosis of myocardial cell was determined by transferase-mediated dUTP nick end labeling (TUNEL) assay, and the expressions of Bcl-2 and Bax were determined by Western blotting. Using network pharmacological analysis, the PI3K/Akt signaling pathway was screened to be associated with both AC and MIRI. Subsequently, the expressions of PI3K, p-Akt and caspase-3 were detected by immunochemistry in myocardial tissues. Results We found that pre-administration of AC improved pain threshold and pathological change of myocardial structure caused by MIRI. AC reduced serum levels of myocardial enzymes and NE in MIRI. Compared with the Sham group, rats in MIRI group showed enhanced oxidative stress levels. These changes were partly reversed by AC. In addition, AC inhibited apoptosis, regulated the expression of apoptosis-related proteins. Immunochemistry analysis confirmed that AC increased the expressions of PI3K and p-Akt in myocardial tissue. Conclusion The cardioprotective effects of AC in MIRI were related with pain alleviation, oxidative stress, apoptosis and sympathetic nerve activity inhibition, the PI3K/Akt signal pathway activation. Clinical trial number Not applicable.https://doi.org/10.1186/s12872-025-04762-0Myocardial ischemia reperfusion injuryActeosideApoptosisThe PI3K/Akt signaling pathwayOxidative stress |
| spellingShingle | Jing Li Yuxin Guo Yang Yang Qing Xue Hong Cao Guangyuan Yang Zhiqi Sun Lin-Lin Jia Hai-Bo Yu The cardioprotective effects of acteoside in myocardial ischemia reperfusion injury and the underlying mechanism BMC Cardiovascular Disorders Myocardial ischemia reperfusion injury Acteoside Apoptosis The PI3K/Akt signaling pathway Oxidative stress |
| title | The cardioprotective effects of acteoside in myocardial ischemia reperfusion injury and the underlying mechanism |
| title_full | The cardioprotective effects of acteoside in myocardial ischemia reperfusion injury and the underlying mechanism |
| title_fullStr | The cardioprotective effects of acteoside in myocardial ischemia reperfusion injury and the underlying mechanism |
| title_full_unstemmed | The cardioprotective effects of acteoside in myocardial ischemia reperfusion injury and the underlying mechanism |
| title_short | The cardioprotective effects of acteoside in myocardial ischemia reperfusion injury and the underlying mechanism |
| title_sort | cardioprotective effects of acteoside in myocardial ischemia reperfusion injury and the underlying mechanism |
| topic | Myocardial ischemia reperfusion injury Acteoside Apoptosis The PI3K/Akt signaling pathway Oxidative stress |
| url | https://doi.org/10.1186/s12872-025-04762-0 |
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