Baicalin improves isoproterenol-induced cardiac remodeling by regulating the Nrf2-dependent signaling pathway
Abstract Background Cardiovascular disease carries the highest mortality rate among diseases, and pharmacological interventions have limited efficacy. Baicalin (Bai) promotes biological metabolic processes, eliminates oxygen free radicals, and is anti-inflammatory. This study aimed to investigate th...
Saved in:
| Main Authors: | , , , , , , , , |
|---|---|
| Format: | Article |
| Language: | English |
| Published: |
BMC
2024-12-01
|
| Series: | BMC Cardiovascular Disorders |
| Subjects: | |
| Online Access: | https://doi.org/10.1186/s12872-024-04395-9 |
| Tags: |
Add Tag
No Tags, Be the first to tag this record!
|
| _version_ | 1850133220103815168 |
|---|---|
| author | Kai Qian Li Song Jia-Min Guo Dan Fu Jia Shi Yu Ma Zi-Jie Ge Lei Li Su-qin Zhang |
| author_facet | Kai Qian Li Song Jia-Min Guo Dan Fu Jia Shi Yu Ma Zi-Jie Ge Lei Li Su-qin Zhang |
| author_sort | Kai Qian |
| collection | DOAJ |
| description | Abstract Background Cardiovascular disease carries the highest mortality rate among diseases, and pharmacological interventions have limited efficacy. Baicalin (Bai) promotes biological metabolic processes, eliminates oxygen free radicals, and is anti-inflammatory. This study aimed to investigate the effect of Bai on the cardiac injury model induced by isoproterenol in mice. Methods and Result In this study, all groups except the control received intraperitoneal injections of isoproterenol (ISO) to induce a cardiac injury model, with the drug administered continuously for 14 days. hematoxylin and eosin staining and Masson’s trichrome staining revealed that Bai significantly mitigated ISO-induced pathological changes in mouse heart tissue and alleviated myocardial hypertrophy. Echocardiography assessments demonstrated that Bai preserved cardiac function in ISO-treated mice. Furthermore, our findings indicated that Bai activated the Nrf2 signaling pathway in vivo and in vitro. To delve deeper, mice were further treated with ML385 (ML) via intraperitoneal injection to inhibit the Nrf2 pathway. Results showed that ML385 blocked the cardioprotective effects of Bai in mouse heart tissue. Conclusion Bai protects against ISO-induced cardiac injury, and its mechanism is related to activating the Nrf2/HO-1 signaling pathway to regulate cardiac ferroptosis and improve cardiac remodeling. |
| format | Article |
| id | doaj-art-13be81587fca49a8ada7bcc52c16dbdd |
| institution | OA Journals |
| issn | 1471-2261 |
| language | English |
| publishDate | 2024-12-01 |
| publisher | BMC |
| record_format | Article |
| series | BMC Cardiovascular Disorders |
| spelling | doaj-art-13be81587fca49a8ada7bcc52c16dbdd2025-08-20T02:32:00ZengBMCBMC Cardiovascular Disorders1471-22612024-12-0124111210.1186/s12872-024-04395-9Baicalin improves isoproterenol-induced cardiac remodeling by regulating the Nrf2-dependent signaling pathwayKai Qian0Li Song1Jia-Min Guo2Dan Fu3Jia Shi4Yu Ma5Zi-Jie Ge6Lei Li7Su-qin Zhang8Department of Cardiology, Key Laboratory of Panvascular Diseases of Wenzhou, The Second Affiliated Hospital and Yuying Children’s Hospital of Wenzhou Medical UniversityMedical College of YiChun UniversityDepartment of Cardiology, Key Laboratory of Panvascular Diseases of Wenzhou, The Second Affiliated Hospital and Yuying Children’s Hospital of Wenzhou Medical UniversityMedical College of YiChun UniversityMedical College of YiChun UniversityMedical College of YiChun UniversityMedical College of YiChun UniversityDepartment of Cardiology, Key Laboratory of Panvascular Diseases of Wenzhou, The Second Affiliated Hospital and Yuying Children’s Hospital of Wenzhou Medical UniversityDepartment of Cardiology, Key Laboratory of Panvascular Diseases of Wenzhou, The Second Affiliated Hospital and Yuying Children’s Hospital of Wenzhou Medical UniversityAbstract Background Cardiovascular disease carries the highest mortality rate among diseases, and pharmacological interventions have limited efficacy. Baicalin (Bai) promotes biological metabolic processes, eliminates oxygen free radicals, and is anti-inflammatory. This study aimed to investigate the effect of Bai on the cardiac injury model induced by isoproterenol in mice. Methods and Result In this study, all groups except the control received intraperitoneal injections of isoproterenol (ISO) to induce a cardiac injury model, with the drug administered continuously for 14 days. hematoxylin and eosin staining and Masson’s trichrome staining revealed that Bai significantly mitigated ISO-induced pathological changes in mouse heart tissue and alleviated myocardial hypertrophy. Echocardiography assessments demonstrated that Bai preserved cardiac function in ISO-treated mice. Furthermore, our findings indicated that Bai activated the Nrf2 signaling pathway in vivo and in vitro. To delve deeper, mice were further treated with ML385 (ML) via intraperitoneal injection to inhibit the Nrf2 pathway. Results showed that ML385 blocked the cardioprotective effects of Bai in mouse heart tissue. Conclusion Bai protects against ISO-induced cardiac injury, and its mechanism is related to activating the Nrf2/HO-1 signaling pathway to regulate cardiac ferroptosis and improve cardiac remodeling.https://doi.org/10.1186/s12872-024-04395-9BaicalinCardiac remodelingNrf2/HO-1FerroptosisIsoproterenol |
| spellingShingle | Kai Qian Li Song Jia-Min Guo Dan Fu Jia Shi Yu Ma Zi-Jie Ge Lei Li Su-qin Zhang Baicalin improves isoproterenol-induced cardiac remodeling by regulating the Nrf2-dependent signaling pathway BMC Cardiovascular Disorders Baicalin Cardiac remodeling Nrf2/HO-1 Ferroptosis Isoproterenol |
| title | Baicalin improves isoproterenol-induced cardiac remodeling by regulating the Nrf2-dependent signaling pathway |
| title_full | Baicalin improves isoproterenol-induced cardiac remodeling by regulating the Nrf2-dependent signaling pathway |
| title_fullStr | Baicalin improves isoproterenol-induced cardiac remodeling by regulating the Nrf2-dependent signaling pathway |
| title_full_unstemmed | Baicalin improves isoproterenol-induced cardiac remodeling by regulating the Nrf2-dependent signaling pathway |
| title_short | Baicalin improves isoproterenol-induced cardiac remodeling by regulating the Nrf2-dependent signaling pathway |
| title_sort | baicalin improves isoproterenol induced cardiac remodeling by regulating the nrf2 dependent signaling pathway |
| topic | Baicalin Cardiac remodeling Nrf2/HO-1 Ferroptosis Isoproterenol |
| url | https://doi.org/10.1186/s12872-024-04395-9 |
| work_keys_str_mv | AT kaiqian baicalinimprovesisoproterenolinducedcardiacremodelingbyregulatingthenrf2dependentsignalingpathway AT lisong baicalinimprovesisoproterenolinducedcardiacremodelingbyregulatingthenrf2dependentsignalingpathway AT jiaminguo baicalinimprovesisoproterenolinducedcardiacremodelingbyregulatingthenrf2dependentsignalingpathway AT danfu baicalinimprovesisoproterenolinducedcardiacremodelingbyregulatingthenrf2dependentsignalingpathway AT jiashi baicalinimprovesisoproterenolinducedcardiacremodelingbyregulatingthenrf2dependentsignalingpathway AT yuma baicalinimprovesisoproterenolinducedcardiacremodelingbyregulatingthenrf2dependentsignalingpathway AT zijiege baicalinimprovesisoproterenolinducedcardiacremodelingbyregulatingthenrf2dependentsignalingpathway AT leili baicalinimprovesisoproterenolinducedcardiacremodelingbyregulatingthenrf2dependentsignalingpathway AT suqinzhang baicalinimprovesisoproterenolinducedcardiacremodelingbyregulatingthenrf2dependentsignalingpathway |