{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"omics_type":["Unknown"],"volume":["14"],"submitter":["Cao Q"],"pubmed_abstract":["<h4>Introduction</h4>The prevalence of ischemic heart disease has reached pandemic levels worldwide. Early revascularization is currently the most effective therapy for ischemic heart diseases but paradoxically induces myocardial ischemia/reperfusion (MI/R) injury. Cardiac inflammatory reaction and oxidative stress are primarily involved in the pathology of MI/R injury. Low-intensity pulsed ultrasound (LIPUS) has been demonstrated to reduce cell injury by protecting against inflammatory reaction and oxidative stress in many diseases, including cardiovascular diseases, but rarely on MI/R injury.<h4>Methods</h4>This study was designed to clarify whether LIPUS alleviates MI/R injury by alleviating inflammatory reaction and oxidative stress. Simultaneously, we have also tried to confirm which intensity of the LIPUS might be more suitable to ameliorate the MI/R injury, as well as to clarify the signaling mechanisms. MI/R and simulated ischemia/reperfusion (SI/R) were respectively induced in Sprague Dawley rats and human pluripotent stem cell-derived cardiomyocytes (hPSC-CMs). LIPUS treatment, biochemical measurements, cell death assay, estimation of cardiac oxidative stress and inflammatory reaction, and protein detections by western blotting were performed according to the protocol.<h4>Results</h4>In our study, both in vivo and in vitro, LIPUS of 0.1 W/cm<sup>2</sup> (LIPUS<sub>0.1</sub>) and 0.5 W/cm<sup>2</sup> (LIPUS<sub>0.5</sub>) make no significant difference in the cardiomyocytes under normoxic condition. Under the hypoxic condition, MI/R injury, inflammatory reaction, and oxidative stress were partially ameliorated by LIPUS<sub>0.5</sub> but were significantly aggravated by LIPUS of 2.5 W/cm<sup>2</sup> (LIPUS<sub>2.5</sub>) both in vivo and in vitro. The activation of the apoptosis signal-regulating kinase 1 (ASK1)/c-Jun N-terminal kinase (JNK) pathway in cardiomyocytes with MI/R injury was partly rectified LIPUS<sub>0.5</sub> both in vivo and in vitro.<h4>Conclusion</h4>Our study firstly demonstrated that LIPUS of different intensities differently affects MI/R injury by regulating cardiac inflammatory reaction and oxidative stress. Modulations on the ASK1/JNK pathway are the signaling mechanism by which LIPUS<sub>0.5</sub> exerts cardioprotective effects. LIPUS<sub>0.5</sub> is promising for clinical translation in protecting against MI/R injury. This will be great welfare for patients suffering from MI/R injury."],"journal":["Frontiers in immunology"],"pagination":["1248056"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC10513435"],"repository":["biostudies-literature"],"pubmed_title":["Low-intensity pulsed ultrasound of different intensities differently affects myocardial ischemia/reperfusion injury by modulating cardiac oxidative stress and inflammatory reaction."],"pmcid":["PMC10513435"],"pubmed_authors":["Liu L","Hu Y","Zhou Q","Chen J","Huang X","Deng Q","Tan T","Cao S","Guo R","Cao Q"],"additional_accession":[]},"is_claimable":false,"name":"Low-intensity pulsed ultrasound of different intensities differently affects myocardial ischemia/reperfusion injury by modulating cardiac oxidative stress and inflammatory reaction.","description":"<h4>Introduction</h4>The prevalence of ischemic heart disease has reached pandemic levels worldwide. Early revascularization is currently the most effective therapy for ischemic heart diseases but paradoxically induces myocardial ischemia/reperfusion (MI/R) injury. Cardiac inflammatory reaction and oxidative stress are primarily involved in the pathology of MI/R injury. Low-intensity pulsed ultrasound (LIPUS) has been demonstrated to reduce cell injury by protecting against inflammatory reaction and oxidative stress in many diseases, including cardiovascular diseases, but rarely on MI/R injury.<h4>Methods</h4>This study was designed to clarify whether LIPUS alleviates MI/R injury by alleviating inflammatory reaction and oxidative stress. Simultaneously, we have also tried to confirm which intensity of the LIPUS might be more suitable to ameliorate the MI/R injury, as well as to clarify the signaling mechanisms. MI/R and simulated ischemia/reperfusion (SI/R) were respectively induced in Sprague Dawley rats and human pluripotent stem cell-derived cardiomyocytes (hPSC-CMs). LIPUS treatment, biochemical measurements, cell death assay, estimation of cardiac oxidative stress and inflammatory reaction, and protein detections by western blotting were performed according to the protocol.<h4>Results</h4>In our study, both in vivo and in vitro, LIPUS of 0.1 W/cm<sup>2</sup> (LIPUS<sub>0.1</sub>) and 0.5 W/cm<sup>2</sup> (LIPUS<sub>0.5</sub>) make no significant difference in the cardiomyocytes under normoxic condition. Under the hypoxic condition, MI/R injury, inflammatory reaction, and oxidative stress were partially ameliorated by LIPUS<sub>0.5</sub> but were significantly aggravated by LIPUS of 2.5 W/cm<sup>2</sup> (LIPUS<sub>2.5</sub>) both in vivo and in vitro. The activation of the apoptosis signal-regulating kinase 1 (ASK1)/c-Jun N-terminal kinase (JNK) pathway in cardiomyocytes with MI/R injury was partly rectified LIPUS<sub>0.5</sub> both in vivo and in vitro.<h4>Conclusion</h4>Our study firstly demonstrated that LIPUS of different intensities differently affects MI/R injury by regulating cardiac inflammatory reaction and oxidative stress. Modulations on the ASK1/JNK pathway are the signaling mechanism by which LIPUS<sub>0.5</sub> exerts cardioprotective effects. LIPUS<sub>0.5</sub> is promising for clinical translation in protecting against MI/R injury. This will be great welfare for patients suffering from MI/R injury.","dates":{"release":"2023-01-01T00:00:00Z","publication":"2023","modification":"2025-04-22T15:26:16.933Z","creation":"2025-04-06T01:24:42.366Z"},"accession":"S-EPMC10513435","cross_references":{"pubmed":["37744362"],"doi":["10.3389/fimmu.2023.1248056"]}}