ArticleBMC cardiovascular disorders2025
The cardioprotective effects of acteoside in myocardial ischemia reperfusion injury and the underlying mechanism.
Article in BMC cardiovascular disorders, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed.
- CD36 is associated with myocardial ischemia-reperfusion-induced renal injury in diabetic rats, accompanied by alterations in the PI3K/Akt/eNOS pathway.Journal of anesthesia and translational medicine · 2026Article
- From copper transport to cuproptosis: emerging therapeutic targets in cardiovascular disease.Molecular and cellular biochemistry · 2026Review
- Acteoside attenuates myocardial ischemia reperfusion injury by inhibiting the NLRP3 inflammasome activity via the PI3K/Akt signaling pathway.Scientific reports · 2026Article
- Article
- Acteoside as a multifunctional natural glycoside: therapeutic potential across various diseases.Inflammopharmacology · 2025Review
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Authors and funding
9 authors.
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Abstract
introductionWe observed the cardioprotective effects of Acteoside (AC) on myocardial ischemia reperfusion injury (MIRI) and discussed the possible mechanisms.
methodsBefore 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.
resultsWe 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.
conclusionThe 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.
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